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1

Schaffer, Stephen, Takashi Ito, Junichi Azuma, Chian Jong, and Jay Kramer. "Mechanisms Underlying Development of Taurine-Deficient Cardiomyopathy." Hearts 1, no. 2 (2020): 86–98. http://dx.doi.org/10.3390/hearts1020010.

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Taurine is a ubiquitous β-amino acid that plays an essential role in ensuring normal mitochondrial and myocardial function. In the mitochondria, taurine reacts with a tRNA forming a 5-taurinomethyluridine conjugate that primarily regulates the biosynthesis of the mitochondria encoded protein, ND6, which serves as a subunit of complex I of the respiratory chain. Impaired formation of the taurine conjugate reduces activity of complex I and plays a central role in the pathophysiology of the mitochondrial disease MELAS (myopathy, encephalopathy, lactic acidosis and stroke-like episodes). The resto
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Laška, Michal, Marie Nováková, and Tibor Stračina. "(Myocardium Remodelling: From Adaptation Mechanisms to Heart Failure Development)." Cor et Vasa 66, no. 1 (2024): 53–64. http://dx.doi.org/10.33678/cor.2023.090.

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Gritsenko, O. V., G. A. Chumakova, I. V. Shevlyakov, and E. V. Trubina. "THE MECHANISMS OF HEART FAILURE DEVELOPMENT IN OBESITY." Russian Journal of Cardiology, no. 5 (June 2, 2018): 81–86. http://dx.doi.org/10.15829/1560-4071-2018-5-81-86.

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Khodjaev, Soidjon D., John R. Teerlink, and Fady I. Malik. "Novel drug mechanisms in development for heart failure." Pflügers Archiv - European Journal of Physiology 466, no. 6 (2014): 1219–25. http://dx.doi.org/10.1007/s00424-014-1528-9.

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5

Mann, Douglas L., and G. Michael Felker. "Mechanisms and Models in Heart Failure." Circulation Research 128, no. 10 (2021): 1435–50. http://dx.doi.org/10.1161/circresaha.121.318158.

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Despite multiple attempts to develop a unifying hypothesis that explains the pathophysiology of heart failure with a reduced ejection fraction (HFrEF), no single conceptual model has withstood the test of time. In the present review, we discuss how the results of recent successful phase III clinical development programs in HFrEF are built upon existing conceptual models for drug development. We will also discuss where recent successes in clinical trials do not fit existing models to identify areas where further refinement of current paradigms may be needed. To provide the necessary structure f
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Ricardo, Daniel Flores Altamirano, Rojas Cruz Gabriela, Alejandro Leal Avalos Omar, Paola Morales Gloria Joanna, and Leticia Torres Martínez Laura. "Unraveling the Complex Pathophysiology of Heart Failure with Preserved Ejection Fraction: Mechanistic Insights and Therapeutic Frontiers." International Journal of Medical Science and Clinical Research Studies 04, no. 07 (2024): 1323–30. https://doi.org/10.5281/zenodo.12699021.

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Heart failure with preserved ejection fraction (HFpEF) represents a significant and growing subset of heart failure cases, characterized by clinical signs and symptoms of heart failure despite a normal or near-normal left ventricular ejection fraction (LVEF). Unlike heart failure with reduced ejection fraction (HFrEF), the pathophysiological mechanisms underlying HFpEF are multifactorial and complex, involving intricate interactions between comorbidities, myocardial structural and functional abnormalities, and systemic inflammatory responses. This review delves into the intricate pathophysiolo
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Dhalla, Naranjan, Vijayan Elimban, Adriana Adameova, and Ramesh Goyal. "Molecular mechanisms for pathophysiology and therapy of cardiac dysfunction in heart failure." Scripta Medica 56, no. 1 (2025): 117–36. https://doi.org/10.5937/scriptamed56-56443.

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Extensive work over the past 6 decades in the field of cardiovascular medicine has revealed that haemodynamic, hormonal, metabolic, cellular and molecular mechanisms of heart failure are not only complex but are also dependent upon the type and stage of heart disease. Although various agents such as b-adrenoreceptor blockers, angiotensin converting enzyme inhibitors, angiotensin II receptor antagonists and vasodilators are available for the treatment of heart failure, these interventions delay the progression of heart failure without reducing mortality and morbidity. In this article, literatur
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Yang, Jian, Wei-wei Xu, and Shen-jiang Hu. "Heart Failure: Advanced Development in Genetics and Epigenetics." BioMed Research International 2015 (2015): 1–11. http://dx.doi.org/10.1155/2015/352734.

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Heart failure (HF) is a complex pathophysiological syndrome that arises from a primary defect in the ability of the heart to take in and/or eject sufficient blood. Genetic mutations associated with familial dilated cardiomyopathy, hypertrophic cardiomyopathy, and arrhythmogenic right ventricular cardiomyopathy can contribute to the various pathologies of HF. Therefore, genetic screening could be an approach for guiding individualized therapies and surveillance. In addition, epigenetic regulation occurs via key mechanisms, including ATP-dependent chromatin remodeling, DNA methylation, histone m
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Caturano, Alfredo, Erica Vetrano, Raffaele Galiero, et al. "Cardiac Hypertrophy: from Pathophysiological Mechanisms to Heart Failure Development." Reviews in Cardiovascular Medicine 23, no. 5 (2022): 165. http://dx.doi.org/10.31083/j.rcm2305165.

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10

Lee, Christopher S. "Mechanisms of Cardiotoxicity and the Development of Heart Failure." Critical Care Nursing Clinics of North America 27, no. 4 (2015): 469–81. http://dx.doi.org/10.1016/j.cnc.2015.07.002.

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11

Ivanchenko, Vera S., Alina A. Gagarina, Irina Ya Goryanskaya, Olga V. Soldatova, and Alexey V. Ushakov. "PATHOGENIC MECHANISMS OF HEART FAILURE IN PATIENTS WITH TYPE 2 DIABETES MELLITUS." Complex Issues of Cardiovascular Diseases 12, no. 4S (2023): 162–72. http://dx.doi.org/10.17802/2306-1278-2023-12-4s-162-172.

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Highlights The review presents up-to-date data on the contribution of type 2 diabetes mellitus to the development and progression of heart failure. The review highlights the key mechanisms of the pathogenesis of heart failure associated with changes in the energy metabolism of cardiomyocytes. AbstractType 2 diabetes mellitus is one of the main risk factors that significantly worsen the prognosis of heart failure and increases the probability of fatal cardiovascular events. The development of heart failure in diabetic patients involves a great number of risk factors for the rapid progression of
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12

Svarovskaya, A. V., and A. A. Garganeeva. "Diabetes mellitus and heart failure — a modern look at the mechanisms of development." Diabetes mellitus 25, no. 3 (2022): 267–74. http://dx.doi.org/10.14341/dm12648.

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Heart failure (HF) is a pressing public health problem. According to the literature, the presence of diabetes mellitus (DM) significantly increases the risk of repeated hospitalizations and the length of hospital stay in patients with heart failure. The proportion of HF remains high due to increased life expectancy, higher prevalence of risk factors and improved survival rates. Currently, advances in the treatment of coronary heart disease (CHD) and valvular disease have significantly improved survival rates, but the prognosis for heart failure remains extremely poor. Among the most important
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Khalirakhmanov, A. F., A. Z. Sharafeev, G. D. Gatiyatullina, S. V. Zinchenko, R. F. Gaifullina, and A. A. Rizvanov. "Heart failure in cancer patients." Siberian journal of oncology 20, no. 6 (2022): 114–19. http://dx.doi.org/10.21294/1814-4861-2021-20-6-114-119.

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The purpose of the study was to conduct a systematic review of data on the role of heart failure (HF) in the development of cancer, as well as to discuss problems dealing with diagnosis and treatment of heart failure in cancer patients. Material and methods. A literature search was conducted using the Cochrane library, elibrary, medline, and embase databases over the past 7 years. The general mechanisms of heart failure and cancer, cardiotoxicity risk factors, and some aspects of the diagnosis and treatment of HF in cancer patients were analyzed. Results. The literature analysis indicates that
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Valaitienė, Julija. "ARRHYTHMIAS IN HEART FAILURE: PATHOPHYSIOLOGY." Health Sciences 35, no. 5 (2024): 201–4. http://dx.doi.org/10.35988/sm-hs.2024.251.

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Heart failure is a medical condition caused by various factors and is associated with significant morbidity and mortality. Significantly, heart failure provokes changes in the expression and regulation of ion channels, leading to electrical remodelling that can increase the risk of arrhythmias. Structural remodelling in heart failure, which involves myocardial hypertrophy, fibrosis, and scar formation, is crucial in the development of arrhythmogenic conditions. This article examines the mechanisms contributing to increased susceptibility to arrhythmias and associated ion channel expression, fu
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Muyassar, Gafurdjanovna Mukhamedova, and Saidjanovna Narzullaeva Dildora. "Optimization of management of patients with chronic heart failure taking into account cardiovascular functional status." GSC Biological and Pharmaceutical Sciences 12, no. 2 (2020): 174–78. https://doi.org/10.5281/zenodo.4268172.

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This review article summarizes the reasons, pathophysiological mechanisms, possible clinical features, and the optimal management strategies of patients with chronic heart failure taking into account cardiovascular functional status. In addition, it shows current situation with chronic heart failure in the world, epidemiological status of the problem as well, risk factors contributing to the development of the disease. 
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16

Bristow, Michael R. "Mechanisms of Development of Heart Failure in the Hypertensive Patient." Cardiology 92, Suppl. 1 (1999): 3–6. http://dx.doi.org/10.1159/000047287.

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17

Efremova, Olga A., Lyudmila A. Kamyshnikova, Natalya I. Obolonkova, Maria S. Sviridova, Tatiana P. Golivets, and Igor I. Khamnagadayev. "Mechanisms of Development of Heart Failure in Chronic Kidney Disease." Актуальные проблемы медицины 45, no. 3 (2022): 237–52. http://dx.doi.org/10.52575/2687-0940-2022-45-3-237-252.

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18

Ostroumova, O. D., and I. V. Goloborodova. "Drug-Induced Heart Failure (Part 2: Mechanisms of Development, Clinical Signs, Differential Diagnosis, Risk Factors, Treatment and Prevention)." Safety and Risk of Pharmacotherapy 8, no. 2 (2020): 57–65. http://dx.doi.org/10.30895/2312-7821-2020-8-2-57-65.

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Heart failure is a complex clinical syndrome caused by an impaired pumping function of the heart muscle, etiologically associated with cardiovascular disease and, in the vast majority of cases, requiring complex therapeutic regimens and simultaneous prescription of several drugs. To date, we know several classes of drugs (including those used for heart failure) which can induce development/progression of heart failure in both patients with left ventricular dysfunction, and in patients who do not have cardiovascular diseases. The aim of the study was to analyse and systematize data on developme
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19

Curcio, Francesco, Gianluca Testa, Ilaria Liguori, et al. "Sarcopenia and Heart Failure." Nutrients 12, no. 1 (2020): 211. http://dx.doi.org/10.3390/nu12010211.

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Modifications of lean mass are a frequent critical determinant in the pathophysiology and progression of heart failure (HF). Sarcopenia may be considered one of the most important causes of low physical performance and reduced cardiorespiratory fitness in older patients with HF. Sarcopenia is frequently misdiagnosed as cachexia. However, muscle wasting in HF has different pathogenetic features in sarcopenic and cachectic conditions. HF may induce sarcopenia through common pathogenetic pathways such as hormonal changes, malnutrition, and physical inactivity; mechanisms that influence each other
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20

Ameer, Syeda Shegufta, Mohammad Bakhtiar Hossain, and Ralph Knöll. "Epigenetics and Heart Failure." International Journal of Molecular Sciences 21, no. 23 (2020): 9010. http://dx.doi.org/10.3390/ijms21239010.

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Epigenetics refers to changes in phenotypes without changes in genotypes. These changes take place in a number of ways, including via genomic DNA methylation, DNA interacting proteins, and microRNAs. The epigenome is the second dimension of the genome and it contains key information that is specific to every type of cell. Epigenetics is essential for many fundamental processes in biology, but its importance in the development and progression of heart failure, which is one of the major causes of morbidity and mortality worldwide, remains unclear. Our understanding of the underlying molecular me
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21

Elendu, Chukwuka, Dependable C. Amaechi, Tochi C. Elendu, et al. "Heart failure and diabetes: Understanding the bidirectional relationship." Medicine 102, no. 37 (2023): e34906. http://dx.doi.org/10.1097/md.0000000000034906.

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Heart failure and diabetes mellitus are 2 common and closely intertwined chronic conditions that often coexist in individuals. The relationship between heart failure and diabetes is bidirectional, meaning that each condition can influence the development and progression of the other. Understanding this complex interplay is crucial for optimizing the management and outcomes of patients with these comorbidities. This review comprehensively analyzed the literature to examine the bidirectional relationship between heart failure and diabetes. We searched various electronic databases and included st
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Riehle, Christian, and Johann Bauersachs. "Small animal models of heart failure." Cardiovascular Research 115, no. 13 (2019): 1838–49. http://dx.doi.org/10.1093/cvr/cvz161.

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Abstract Heart disease is a major cause of death worldwide with increasing prevalence, which urges the development of new therapeutic strategies. Over the last few decades, numerous small animal models have been generated to mimic various pathomechanisms contributing to heart failure (HF). Despite some limitations, these animal models have greatly advanced our understanding of the pathogenesis of the different aetiologies of HF and paved the way to understanding the underlying mechanisms and development of successful treatments. These models utilize surgical techniques, genetic modifications,
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23

Mostafa, Q. Alshamiri. "Diabetic Cardiomyopathy Pathophysiology and Update on Treatment." Global Advanced Research Journal of Medicine and Medical Sciences (ISSN: 2315-5159) 8, no. 4 (2019): 020–27. https://doi.org/10.5281/zenodo.3558862.

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<strong>The presence of diabetes in HF patients portends worse prognosis than does HF without DM. Heart failure in diabetes mellitus (DM) in the absence of conventional risk factors such as hypertension, coronary artery disease (CAD), and congenital or valvular heart disease, has been defined in the literature as diabetic cardiomyopathy (DCM). The question what are the link between DM and DCM? The answer of this question is not well understood. This review will identify the link between diabetes mellitus and DCM, will also explore the possible mechanisms and triggering factors or associations
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Keppner, Lea, Margarete Heinrichs, Max Rieckmann, et al. "Antibodies aggravate the development of ischemic heart failure." American Journal of Physiology-Heart and Circulatory Physiology 315, no. 5 (2018): H1358—H1367. http://dx.doi.org/10.1152/ajpheart.00144.2018.

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Heart-specific antibodies have been widely associated with myocardial infarction (MI). However, it remains unclear whether autoantibodies mediate disease progression or are a byproduct of cardiac injury. To disambiguate the role of immunoglobulins in MI, we characterized the development of ischemic heart failure in agammaglobulinemic mice (AID−/−μS−/−). Although these animals can produce functional B cells, they cannot synthesize secretory IgM (μS−/−) or perform Ig class switching (AID−/−), leading to complete antibody deficiency. Agammaglobulinemia did not affect overall post-MI survival but
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Dardiotis, Efthimios, Gregory Giamouzis, Dimos Mastrogiannis, et al. "Cognitive Impairment in Heart Failure." Cardiology Research and Practice 2012 (2012): 1–9. http://dx.doi.org/10.1155/2012/595821.

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Cognitive impairment (CI) is increasingly recognized as a common adverse consequence of heart failure (HF). Although the exact mechanisms remain unclear, microembolism, chronic or intermittent cerebral hypoperfusion, and/or impaired cerebral vessel reactivity that lead to cerebral hypoxia and ischemic brain damage seem to underlie the development of CI in HF. Cognitive decline in HF is characterized by deficits in one or more cognition domains, including attention, memory, executive function, and psychomotor speed. These deficits may affect patients’ decision-making capacity and interfere with
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Wehrens, Xander H. T. "Unraveling the Mechanisms by Which Calpain Inhibition Prevents Heart Failure Development." JACC: Basic to Translational Science 3, no. 4 (2018): 518–20. http://dx.doi.org/10.1016/j.jacbts.2018.07.002.

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Kraus, Lindsay. "Targeting Epigenetic Regulation of Cardiomyocytes through Development for Therapeutic Cardiac Regeneration after Heart Failure." International Journal of Molecular Sciences 23, no. 19 (2022): 11878. http://dx.doi.org/10.3390/ijms231911878.

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Cardiovascular diseases are the leading cause of death globally, with no cure currently. Therefore, there is a dire need to further understand the mechanisms that arise during heart failure. Notoriously, the adult mammalian heart has a very limited ability to regenerate its functional cardiac cells, cardiomyocytes, after injury. However, the neonatal mammalian heart has a window of regeneration that allows for the repair and renewal of cardiomyocytes after injury. This specific timeline has been of interest in the field of cardiovascular and regenerative biology as a potential target for adult
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Biondi, Bernadette. "MECHANISMS IN ENDOCRINOLOGY: Heart failure and thyroid dysfunction." European Journal of Endocrinology 167, no. 5 (2012): 609–18. http://dx.doi.org/10.1530/eje-12-0627.

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ContextHeart failure (HF) is a major cause of morbidity and mortality in Europe and in the United States. The aim of this review article was to assess the results of the prospective studies that evaluated the risk of HF in patients with overt and subclinical thyroid disease and discuss the mechanism of this dysfunction.Evidence AcquisitionReports published with the following search terms were searched:, thyroid, hypothyroidism, hyperthyroidism, subclinical hyperthyroidism, subclinical hypothyroidism, levothyroxine, triiodothyronine, antithyroid drugs, radioiodine, deiodinases, clinical symptom
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Kanazirev, Branimir. "Heart failure with preserved ejection fraction – new elements of evidence in the field of pathophysiology and new treatment options." Bulgarian Cardiology 27, no. (2) (2021): 84–101. https://doi.org/10.3897/bgcardio.27.e69592.

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Consistent with the understanding of the comorbidity-infl ammation relationship, concomitant diseases and especially metabolic comorbidities are thought to stimulate the development and severity of heart failure with preserved ejection fraction through a cascade of mechanisms supporting systemic tissue infl ammation leading to myocardial fi brosis. Recently, new experimental and clinical evidence has emerged that enhances validity and verifi es the infl ammatory-profi brotic paradigm. This evidence consists of: (1) myocardial infi ltration with immunocompetent cells not only due to metabolic l
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Tsigkou, Vasiliki, Evangelos Oikonomou, Artemis Anastasiou, et al. "Molecular Mechanisms and Therapeutic Implications of Endothelial Dysfunction in Patients with Heart Failure." International Journal of Molecular Sciences 24, no. 5 (2023): 4321. http://dx.doi.org/10.3390/ijms24054321.

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Heart failure is a complex medical syndrome that is attributed to a number of risk factors; nevertheless, its clinical presentation is quite similar among the different etiologies. Heart failure displays a rapidly increasing prevalence due to the aging of the population and the success of medical treatment and devices. The pathophysiology of heart failure comprises several mechanisms, such as activation of neurohormonal systems, oxidative stress, dysfunctional calcium handling, impaired energy utilization, mitochondrial dysfunction, and inflammation, which are also implicated in the developmen
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Gallo, Giovanna, Speranza Rubattu, and Massimo Volpe. "Mitochondrial Dysfunction in Heart Failure: From Pathophysiological Mechanisms to Therapeutic Opportunities." International Journal of Molecular Sciences 25, no. 5 (2024): 2667. http://dx.doi.org/10.3390/ijms25052667.

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Mitochondrial dysfunction, a feature of heart failure, leads to a progressive decline in bioenergetic reserve capacity, consisting in a shift of energy production from mitochondrial fatty acid oxidation to glycolytic pathways. This adaptive process of cardiomyocytes does not represent an effective strategy to increase the energy supply and to restore the energy homeostasis in heart failure, thus contributing to a vicious circle and to disease progression. The increased oxidative stress causes cardiomyocyte apoptosis, dysregulation of calcium homeostasis, damage of proteins and lipids, leakage
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Kario, Kazuomi, and Bryan Williams. "Nocturnal Hypertension and Heart Failure: Mechanisms, Evidence, and New Treatments." Hypertension 78, no. 3 (2021): 564–77. http://dx.doi.org/10.1161/hypertensionaha.121.17440.

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Heart failure (HF) is a common condition with an increasing prevalence. Despite a variety of evidence-based treatments for patients with HF with reduced ejection fraction, morbidity and mortality rates remain high. Furthermore, there are currently no treatments that have yet been shown to reduce complication and death rates in patients who have HF with preserved ejection fraction. Hypertension is a common comorbidity in patients with HF, contributing to disease development and prognosis. For example, hypertension is closely associated with the development of left ventricular hypertrophy, which
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Schirone, Leonardo, Maurizio Forte, Silvia Palmerio, et al. "A Review of the Molecular Mechanisms Underlying the Development and Progression of Cardiac Remodeling." Oxidative Medicine and Cellular Longevity 2017 (2017): 1–16. http://dx.doi.org/10.1155/2017/3920195.

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Pathological molecular mechanisms involved in myocardial remodeling contribute to alter the existing structure of the heart, leading to cardiac dysfunction. Among the complex signaling network that characterizes myocardial remodeling, the distinct processes are myocyte loss, cardiac hypertrophy, alteration of extracellular matrix homeostasis, fibrosis, defective autophagy, metabolic abnormalities, and mitochondrial dysfunction. Several pathophysiological stimuli, such as pressure and volume overload, trigger the remodeling cascade, a process that initially confers protection to the heart as a
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Harutyunyan, K. R., K. V. Melkumyan, H. T. Abrahamyam, S. H. Adamyan, D. H. Khudaverdyan, and A. S. Ter-Markosyan. "Calcium-regulating hormonal system in cardiac functional activity." NEW ARMENIAN MEDICAL JOURNAL, no. 4 (2022): 54–63. http://dx.doi.org/10.56936/18290825-2022.16.4-54.

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The variance of calcium homeostasis is known as a risk factor for the development of heart failure. A study of calcium-regulating hormones is a crucial element to understand underlying pathophysiological mechanisms of heart failure. Pro-inflammatory factors, released during mechanical, hypoxic or bacterial damage of myocardial cells, lead to an imbalance of calcium and disrupt to heart function. The investigation of mentioned factors influence mechanism on the heart, is an urgent solution for preventing the development of heart failure. Present study aimed to reveal the role of calcium-regulat
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Mollanoori, Hasan, Yazdan Rahmati, Bita Hassani, Sajjad Esmaeili, Komail Amini, and Shahram Teimourian. "Screening the underlying molecular mechanisms involved in the development of heart failure." Meta Gene 25 (September 2020): 100743. http://dx.doi.org/10.1016/j.mgene.2020.100743.

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Markel, Troy A., George M. Wairiuko, Tim Lahm, et al. "The Right Heart and Its Distinct Mechanisms of Development, Function, and Failure." Journal of Surgical Research 146, no. 2 (2008): 304–13. http://dx.doi.org/10.1016/j.jss.2007.04.003.

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Buziashvili, Yuri I., Elmira U. Asymbekova, Elvina F. Tugeeva, Akmal Z. Rakhimov, Lusine S. Shakhnazaryan, and Firdavsdzhon R. Akildzhonov. "Molecular mechanisms of inflammation in the development of heart failure: A review." Consilium Medicum 25, no. 10 (2024): 679–84. http://dx.doi.org/10.26442/20751753.2023.10.202433.

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Cardiovascular diseases continue to be the main cause of hospital mortality and lead to great disability of the working population. Numerous clinical and experimental studies have shown that inflammation is the main factor causing the growth and progression of atherosclerosis. Despite significant progress in basic therapy aimed at both preventing the development of heart failure (HF) and treating it, the prognosis in patients after their first hospitalization remains extremely unfavorable. HF is the leading cause of morbidity and mortality worldwide. Various stimuli at different stages of HF p
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Tokmachev, R. E., A. V. Budnevsky, A. Y. Kravchenko, Y. S. Shkatova, T. A. Chernik, and Y. A. Krasnikova. "The Effect of Hypothyroidism on the Development and course of Heart Failure." Pakistan Journal of Medical and Health Sciences 15, no. 5 (2021): 1445–48. http://dx.doi.org/10.53350/pjmhs211551445.

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Thyroid gland dysfunction is a risk factor for development of cardiovascular diseases. From all types of thyroid gland dysfunction hypothyroidism is the most common. Increasing of thyroid-stimulating hormone level can influence the clinical course of chronic heart failure (CHF) because of its extrathyroid effects - namely - influence on lipide metabolism, endothelial function of vessels and blood pressure. Also CHF itself can make negative impact on a thyroid gland functioning, therefore pathophysiological "vicious circle" is formed. Manifest hypothyroidism is associated with an increased risk
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Shah, Anureet K., Sukhwinder K. Bhullar, Vijayan Elimban, and Naranjan S. Dhalla. "Oxidative Stress as A Mechanism for Functional Alterations in Cardiac Hypertrophy and Heart Failure." Antioxidants 10, no. 6 (2021): 931. http://dx.doi.org/10.3390/antiox10060931.

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Although heart failure due to a wide variety of pathological stimuli including myocardial infarction, pressure overload and volume overload is associated with cardiac hypertrophy, the exact reasons for the transition of cardiac hypertrophy to heart failure are not well defined. Since circulating levels of several vasoactive hormones including catecholamines, angiotensin II, and endothelins are elevated under pathological conditions, it has been suggested that these vasoactive hormones may be involved in the development of both cardiac hypertrophy and heart failure. At initial stages of patholo
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Tsutsui, Hiroyuki, Shintaro Kinugawa, and Shouji Matsushima. "Oxidative stress and heart failure." American Journal of Physiology-Heart and Circulatory Physiology 301, no. 6 (2011): H2181—H2190. http://dx.doi.org/10.1152/ajpheart.00554.2011.

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Oxidative stress, defined as an excess production of reactive oxygen species (ROS) relative to antioxidant defense, has been shown to play an important role in the pathophysiology of cardiac remodeling and heart failure (HF). It induces subtle changes in intracellular pathways, redox signaling, at lower levels, but causes cellular dysfunction and damage at higher levels. ROS are derived from several intracellular sources, including mitochondria, NAD(P)H oxidase, xanthine oxidase, and uncoupled nitric oxide synthase. The production of ROS is increased within the mitochondria from failing hearts
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Raza, Shafaat, and Shahzeen Allah Ditto. "Hypochloremia in heart failure: A new prognostic and therapeutic aspect of refractory heart failure." Brain & Heart 2, no. 1 (2024): 2257. http://dx.doi.org/10.36922/bh.2257.

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Heart failure (HF) is one of the most common cardiovascular diseases, bearing a significant burden of morbidity, mortality, and disability. Low serum chloride (Cl) levels have been observed to play an important role in predicting mortality and planning management strategies for HF. This review aims to investigate the influence of hypochloremia on individuals suffering from HF and its correlation with various underlying pathophysiological mechanisms. We conducted a literature review of articles published in the past 10 years, employing specific keywords to identify relevant studies from databas
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Kravchenko, A. Ya, A. V. Budnevskiy, and M. S. Kuzina. "Hypothyroidism and heart failure." Clinical Medicine (Russian Journal) 96, no. 5 (2018): 397–400. http://dx.doi.org/10.18821/0023-2149-2018-96-5-397-400.

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The article is a review of the literature, which presents the results of experimental and clinical studies, meta-analysis data on the effects of hypothyroidism on the clinical course of heart failure, the association between hypothyroidism and clinical outcomes in patients with heart failure. Thyroid gland dysfunction is a risk factor for development of cardiovascular diseases. From all types of thyroid gland dysfunction hypothyroidism is the most common. Increasing of thyroid-stimulating hormone level (which happens in patients with hypothyroidism) can influence the clinical course of chronic
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43

Egom, Emmanuel E., Tiam Feridooni, Adam Hotchkiss, Peter Kruzliak, and Kishore B. S. Pasumarthi. "Mechanisms of renal hyporesponsiveness to BNP in heart failure." Canadian Journal of Physiology and Pharmacology 93, no. 6 (2015): 399–403. http://dx.doi.org/10.1139/cjpp-2014-0356.

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The B-type natriuretic peptide (BNP), a member of the family of vasoactive peptides, is a potent natriuretic, diuretic, and vasodilatory peptide that contributes to blood pressure and volume homeostasis. These attributes make BNP an ideal drug that could aid in diuresing a fluid-overloaded patient who had poor or worsening renal function. Despite the potential benefits of BNP, accumulating evidence suggests that simply increasing the amount of circulating BNP does not necessarily increase natriuresis in patients with heart failure (HF). Moreover, despite high BNP levels, natriuresis falls when
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44

Masenga, Sepiso K., Joreen P. Povia, Propheria C. Lwiindi, and Annet Kirabo. "Recent Advances in Microbiota-Associated Metabolites in Heart Failure." Biomedicines 11, no. 8 (2023): 2313. http://dx.doi.org/10.3390/biomedicines11082313.

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Heart failure is a risk factor for adverse events such as sudden cardiac arrest, liver and kidney failure and death. The gut microbiota and its metabolites are directly linked to the pathogenesis of heart failure. As emerging studies have increased in the literature on the role of specific gut microbiota metabolites in heart failure development, this review highlights and summarizes the current evidence and underlying mechanisms associated with the pathogenesis of heart failure. We found that gut microbiota-derived metabolites such as short chain fatty acids, bile acids, branched-chain amino a
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45

Begrambekova, Yu L., N. A. Karanadze, and Ya A. Orlova. "Alterations of the respiratory system in heart failure." Kardiologiia 59, no. 2S (2019): 15–24. http://dx.doi.org/10.18087/cardio.2626.

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The review discusses mechanisms for the development of the pathology of the respiratory system in patients with CHF, such as various types of periodic respiration, pulmonary hypertension due to the pathology of the left chambers of the heart, and remodeling of the respiratory musculature. The role of chemo- and baroreceptors of the carotid zone, as well as the hyperactivation of the respiratory muscle metaboreflex in the development of the pathology of the respiratory system, and the mediated exacerbation of CHF are discussed.
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46

Sygitowicz, Grażyna, and Dariusz Sitkiewicz. "Involvement of circRNAs in the Development of Heart Failure." International Journal of Molecular Sciences 23, no. 22 (2022): 14129. http://dx.doi.org/10.3390/ijms232214129.

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In recent years, interest in non-coding RNAs as important physiological regulators has grown significantly. Their participation in the pathophysiology of cardiovascular diseases is extremely important. Circular RNA (circRNA) has been shown to be important in the development of heart failure. CircRNA is a closed circular structure of non-coding RNA fragments. They are formed in the nucleus, from where they are transported to the cytoplasm in a still unclear mechanism. They are mainly located in the cytoplasm or contained in exosomes. CircRNA expression varies according to the type of tissue. In
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47

Fonseka, Oveena, Sanskruti Ravindra Gare, Xinyi Chen, et al. "Molecular Mechanisms Underlying Heart Failure and Their Therapeutic Potential." Cells 14, no. 5 (2025): 324. https://doi.org/10.3390/cells14050324.

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Heart failure (HF) is a prominent fatal cardiovascular disorder afflicting 3.4% of the adult population despite the advancement of treatment options. Therefore, a better understanding of the pathogenesis of HF is essential for exploring novel therapeutic strategies. Hypertrophy and fibrosis are significant characteristics of pathological cardiac remodeling, contributing to HF. The mechanisms involved in the development of cardiac remodeling and consequent HF are multifactorial, and in this review, the key underlying mechanisms are discussed. These have been divided into the following categorie
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48

Patel, Yash, and Jacob Joseph. "Sodium Intake and Heart Failure." International Journal of Molecular Sciences 21, no. 24 (2020): 9474. http://dx.doi.org/10.3390/ijms21249474.

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Sodium is an essential mineral and nutrient used in dietary practices across the world and is important to maintain proper blood volume and blood pressure. A high sodium diet is associated with increased expression of β—myosin heavy chain, decreased expression of α/β—myosin heavy chain, increased myocyte enhancer factor 2/nuclear factor of activated T cell transcriptional activity, and increased salt-inducible kinase 1 expression, which leads to alteration in myocardial mechanical performance. A high sodium diet is also associated with alterations in various proteins responsible for calcium ho
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Henriksen, Peter A. "Anthracycline cardiotoxicity: an update on mechanisms, monitoring and prevention." Heart 104, no. 12 (2017): 971–77. http://dx.doi.org/10.1136/heartjnl-2017-312103.

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Anthracycline chemotherapy causes dose-related cardiomyocyte injury and death leading to left ventricular dysfunction. Clinical heart failure may ensue in up to 5% of high-risk patients. Improved cancer survival together with better awareness of the late effects of cardiotoxicity has led to growing recognition of the need for surveillance of anthracycline-treated cancer survivors with early intervention to treat or prevent heart failure. The main mechanism of anthracycline cardiotoxicity is now thought to be through inhibition of topoisomerase 2β resulting in activation of cell death pathways
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Li, Jia, Peter Moritz Becher, Stefan Blankenberg, and Dirk Westermann. "Current Treatment of Heart Failure with Preserved Ejection Fraction: Should We Add Life to the Remaining Years or Add Years to the Remaining Life?" Cardiology Research and Practice 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/130724.

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According to the ejection fraction, patients with heart failure may be divided into two different groups: heart failure with preserved or reduced ejection fraction. In recent years, accumulating studies showed that increased mortality and morbidity rates of these two groups are nearly equal. More importantly, despite decline in mortality after treatment in regard to current guideline in patients with heart failure with reduced ejection fraction, there are still no trials resulting in improved outcome in patients with heart failure with preserved ejection fraction so far. Thus, novel pathophysi
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