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Rozprawy doktorskie na temat „Reverse cholesterol transport pathway”

Autor: Grafiati

Data publikacji: 2 czerwca 2025

Data aktualizacji: 31 lipca 2025

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1

Catalano, Giovanna. "Role of HDL particles in the reverse cholesterol transport pathway : a clinical need to evaluate HDL functionality." Paris 6, 2008. http://www.theses.fr/2008PA066420.

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Les taux de cholestérol-HDL (C-HDL) représentent un facteur de risque indépendant de maladie cardiovasculaire et des taux élèves de C-HDL sont corrélés à une diminution du risque cardiovasculaire. Dans le contexte du transport inverse du cholestérol, la sortie du cholestérol des cellules et la délivrance des esters de cholestérol au niveau hépatique représentent les étapes majeures impliquant les particules HDL. Au cours des dyslipidémies athérogènes les concentrations plasmatiques de C-HDL ainsi que la distribution du cholestérol au sein des sous populations de HDL sont altérés. La protéine c

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2

Zhou, Huali. "Reverse cholesterol transport in type 2 diabetes mellitus." Click to view the E-thesis via HKUTO, 2008. http://sunzi.lib.hku.hk/hkuto/record/B39794003.

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Zhou, Huali, and 周華麗. "Reverse cholesterol transport in type 2 diabetes mellitus." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2008. http://hub.hku.hk/bib/B39794003.

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4

Cooke, Conrad Martin. "Investigation of reverse cholesterol transport in humans in vivo." Thesis, Queen Mary, University of London, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.405731.

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5

Sabeva, Nadezhda Steliyanova. "REGULATION OF ABCG5 AND ABCG8 STEROL TRANSPORTERS IN BILIARY CHOLESTEROL ELIMINATION, REVERSE CHOLESTEROL TRANSPORT AND DYSLIPIDEMIA." UKnowledge, 2011. http://uknowledge.uky.edu/gradschool_diss/193.

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ATP-binding cassette transporters ABCA1 and ABCG1 initiate reverse cholesterol transport generating HDL particles, whereas ABCG5/G8 promote biliary cholesterol secretion thereby facilitating the last step of reverse cholesterol transport. Mutations in the leptin axis result in obesity and dyslipidemia in ob/ob and db/db mice. These mice have defective HDL clearance, increased plasma cholesterol and decreased biliary cholesterol elimination. My studies demonstrate that ABCG5/G8 protein is low in these animals and can be restored with caloric restriction or leptin replacement. To directly test w

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6

Teh, Evelyn Mei-lin. "Molecular defects and structure/function studies of proteins in reverse cholesterol transport." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0017/NQ57371.pdf.

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7

Shen, Haiqing. "New candidate gene involved in reverse cholesterol transport (RCT) : the case for phospholipid transfer protein (PLTP): interactions with dietary factors /." Thesis, Connect to Dissertations & Theses @ Tufts University, 2004.

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Thesis (Ph.D.)--Tufts University, 2004.<br>Adviser: Jose Ordovas. Submitted to the School of Nutrition Science and Policy. Includes bibliographical references (leaves 136-137). Access restricted to members of the Tufts University community. Also available via the World Wide Web;

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8

Sparks, Daniel Leslie. "The effect of variations in HDL composition on components of reverse cholesterol transport." Thesis, University of British Columbia, 1989. http://hdl.handle.net/2429/29290.

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This thesis is concerned with the mechanism which underlies the apparent anti-atherogenic capacity of high density lipoproteins (HDL). Specifically, the relationship between HDL composition, cholesteryl ester transfer protein (CETP) and lecithin: cholesterol acyltransferase (LCAT) was investigated. A novel assay was developed which allowed for the determination of the rate of transfer of [³H]cholesteryl ester from agarose-bound HDL to the endogenous lipoproteins of a plasma sample. Comparison of this assay with an established method, which utilized exogenous lipoprotein substrates, indicated

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9

Al-Khfajy, Wrood Salim Dawood. "Role Of Transmembrane 141 in Cholesterol Metabolism." Kent State University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=kent1416142859.

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10

Mindham, Malcolm A. "Development, validation and application of the isolated perfused rat spleen for the study of reverse cholesterol transport." Thesis, Royal Veterinary College (University of London), 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.522691.

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11

Altemus, Jessica B. "Induction of Liver Abcg5/Abcg8 Expression is an Important Determinant of the Macrophage-to-Feces Reverse Cholesterol Transport Response to Treatment with Ezetimibe." Cleveland State University / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=csu1366662840.

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12

Wang, Yuhuan. "ROLES OF ABCG5 ABCG8 CHOLESTEROL TRANSPORTER IN LIPID HOMEOSTASIS." UKnowledge, 2015. http://uknowledge.uky.edu/pharmacy_etds/50.

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The ABCG5 ABCG8 (G5G8) sterol transporter promotes cholesterol secretion into bile and opposes dietary sterol absorption in the small intestine. An emerging body of literature suggests that G5G8 links sterol flux to various risk factors for metabolic syndrome (MetS) and nonalcoholic fatty liver disease (NAFLD). Therapeutic approaches that accelerate G5G8 activity may augment reverse cholesterol transport (RCT) and provide beneficial effects in the prevention and treatment of cardiovascular and liver disease. Mice lacking leptin (ob/ob) or its receptor (db/db) are obese, insulin resistant in pa

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13

Fragoso, Yara Dadalti. "The role of subfractions of high density lipoprotein in reverse cholesterol transport : the rabbit as an experimental model." Thesis, University of Aberdeen, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.386319.

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Coronary heart disease (CHD) is a major cause of death and incapacitation. CHD may arise after decades of degenerative disease in the arteries, where cholesterol is deposited. The only alternative for the removal of cholesterol from the arteries, and therefore prevention of long-term lesions, is "reverse cholesterol transport" (RCT), a mechanism mediated by high density lipoprotein (HDL). The present thesis was concerned with the role of specific subfractions of HDL which are relevant to RCT. In this study, the rabbit was proven to be a very good model, with similar lipid and HDL profile to hu

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14

Paranjape, Sulabha. "Studies of the Interaction of LCAT with Lipoprotein Substrates in HDL Deficient Plasma Systems." Thesis, University of North Texas, 1989. https://digital.library.unt.edu/ark:/67531/metadc500446/.

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Enzymatic and lipid transfer reactions involved in reverse cholesterol transport were studied in HDL deficient plasma systems. Fasting plasma samples were obtained from control and cholesterol fed guinea pigs as well as from a fish eye disease patient and were used to localize the enzyme LCAT among plasma lipoproteins (VLDL, LDL, and HDL). In both guinea pig and fish eye disease patient plasma, the LCAT activity was found in association with the HDL type particles. Cholesterol feeding in guinea pigs altered the properties of lipoprotein substrates for LCAT resulting in some changes, specifical

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15

Lee, Myoung-Sook. "Differential effects of dietary polyunsaturated fat on the reverse cholesterol transport mechanisms according to the Apo E isoforms in normolipidemic females /." The Ohio State University, 1993. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487843688959297.

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16

Bowden, Kristin Louise. "The role of lysosomal acid lipase in regulation of the ATP-binding cassette transporter A1, high density lipoprotein and reverse cholesterol transport." Thesis, University of British Columbia, 2013. http://hdl.handle.net/2429/45369.

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The key regulator of initial HDL particle formation by cells is the ATP-binding cassette transporter A1 (ABCA1). ABCA1 expression is regulated primarily by oxysterol dependent activation of the liver X receptor (LXR). We investigated the role of lysosomal cholesterol on ABCA1 regulation by studying the lysosomal disorder Cholesteryl Ester Storage Disease (CESD). CESD is caused by genetic mutations in the LIP-A gene that result in only 5% of normal activity of lysosomal acid lipase (LAL), an enzyme that hydrolyzes cholesteryl esters (CE) and triglycerides on internalized lipoproteins specifica

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17

Dubois, Denis. "Contribution à l'étude du métabolisme des HDL chez l'être humain: mise en évidence des fonctions spécifiques des HDL en dehors du "reverse cholesterol transport"." Doctoral thesis, Universite Libre de Bruxelles, 1993. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/212863.

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18

Espinosa, Delgado Sara. "Contribution respective des récepteurs P2Y13 et SR-BI dans le métabolisme du HDL-C et le développement de l'athérosclérose." Thesis, Toulouse 3, 2017. http://www.theses.fr/2017TOU30053.

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L’effet athéroprotecteur des Lipoprotéines de Haute Densité (HDL) est principalement attribué à leur rôle clé dans Transport Retour du Cholestérol (RCT), un processus par lequel le cholestérol excédentaire des cellules périphériques est capté par les particules HDL pour être amené au foie où il sera préférentiellement sécrété dans les voies biliaires, puis excrété dans les fèces. Deux voies indépendantes ont été identifiées comme étant impliquées dans l’endocytose hépatique du HDL. La première est la voie ecto-F1-ATPase/P2Y13 dans laquelle l’apoA-I (apolipoprotéine majoritaire des HDL) se lie

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19

Koeth, Robert Alden. "DIETARY TRIMETHYLAMINES, THE GUT MICROBIOTA,AND ATHEROSCLEROSIS." Case Western Reserve University School of Graduate Studies / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=case1369997123.

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20

Okuda, Ligia Shimabukuro. "Albumina modificada por glicação avançada sensibiliza macrófagos à inflamação prejudicando o transporte reverso de colesterol e a atividade anti-inflamatória da HDL." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/5/5135/tde-30072012-082700/.

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No diabete melito, produtos de glicação avançada (AGE) reduzem o efluxo de colesterol celular o que agrava o desenvolvimento da aterosclerose. Neste estudo, investigou-se o papel da albumina modificada por glicação avançada (albumina-AGE) sobre a sensibilização de macrófagos à resposta inflamatória e o impacto da secreção de citocinas, quimocinas e moléculas de adesão sobre o efluxo de colesterol mediado por apolipoproteína A-I e subfrações de HDL. Além disso, determinou-se a capacidade da HDL em modular a resposta inflamatória em macrófagos tratados com albumina-AGE. Macrófagos de peritônio d

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21

Genvigir, Fabiana Dalla Vecchia. "Efeito de hipolipemiantes sobre a expressão de genes envolvidos no transporte reverso do colesterol." Universidade de São Paulo, 2011. http://www.teses.usp.br/teses/disponiveis/9/9136/tde-20122011-233808/.

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A eficácia das estatinas em reduzir o risco de eventos coronarianos não é completamente explicada por seus efeitos em diminuir colesterol de lipoproteína de baixa densidade (LDL-C). Um dos seus efeitos adicionais pode ser decorrente da modificação na concentração de lipoproteína de alta densidade (HDL), reconhecida como ateroprotetora, principalmente por seu papel no transporte reverso do colesterol (TRC). Os transportadores de membrana do tipo ATP-binding cassette, ABCA1 e ABCG1, e o scavenger receptor BI (SRBI) são proteínas importantes envolvidas no TRC e seus genes são regulados por vários

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22

Gall, Julie. "Physiopathologie de l'efflux de cholestérol du macrophage humain : relation avec le développement de l'athérosclérose et la mortalité chez des patients à haut risque cardiovasculaire." Thesis, Paris 6, 2017. http://www.theses.fr/2017PA066019.

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La capacité des particules HDL à exercer des effets anti-athérogènes passe notamment par leur capacité à assurer le transport inverse du cholestérol (RCT). L'objectif principal de mon programme de recherche est l'étude de l'étape initiale du transport inverse du cholestérol que représente l'efflux de cholestérol du macrophage, dans le contexte des maladies métaboliques et du risque cardiovasculaire et de mortalité. J'ai étudié la relation entre l'efflux, et les conséquences sur le développement de l'athérosclérose dans un contexte métabolique particulier ; le syndrome métabolique (SM). J'ai dé

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23

Lee, Samuel. "Insulin Regulation of Reverse Cholesterol Transport." Thesis, 2019. https://doi.org/10.7916/d8-yzmw-9347.

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Insulin resistance and type 2 diabetes are pathogenetically linked to increased risk of cardiovascular disease. While insulin resistance is defined by a dysregulation in hepatic insulin signaling, it is unclear how this impairment relates to the development of cardiovascular disease. Recently, there has been evidence showing that in insulin resistant individuals, cardiovascular disease is associated with a defect in reverse cholesterol transport – the cardioprotective process by which excess cholesterol is removed from the periphery, and returned to the liver for biliary excretion. Reverse cho

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24

Lien, Chi-Li, and 連致力. "The Role of Quercetin in Reverse Cholesterol Transport." Thesis, 2008. http://ndltd.ncl.edu.tw/handle/17852253923721408415.

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碩士<br>國立陽明大學<br>生化暨分子生物研究所<br>96<br>Accumulated evidence indicate that quercetin, the major flavonol in the plant kingdom, may possess beneficial effects in atherosclerosis. The protective effects of quercetin on the development of atherosclerosis include anti-inflammatory, anti-oxidative, anti-thrombotic and anti-proliferative activities. However, the mechanism of quercetin on reverse cholesterol transport remains unclear. High density-lipoprotein (HDL) have been attributed to a role in reverse cholesterol transport, especially the macrophage-dependent pathway. Apolipoprotein A1 (apoA-1) and

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25

Sengupta, Bhaswati. "Validation of a novel hypothesis of generating foam cells by its use to study reverse cholesterol transport." Doctoral diss., 2014. http://digital.library.ucf.edu/cdm/ref/collection/ETD/id/6176.

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Generation of foam cells, an essential step for reverse cholesterol transport (RCT) studies, uses the technique of receptor dependent macrophage loading with radiolabeled acetylated Low Density Lipoprotein (Ac-LDL). In this study, we used the ability of a biologically relevant detergent molecule, Lysophosphatidylcholine (Lyso PtdCho), to form mixed micelles with cholesterol or cholesteryl ester (CE) to generate macrophage foam cells. Fluorescent or radiolabelled cholesterol / Lyso PtdCho mixed micelles were prepared and incubated with RAW 264.7 or mouse peritoneal macrophages. Results showed t

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26

Bujold, Kim. "Régulation du métabolisme et du transport des lipides dans les macrophages : potentiel anti-athérosclérotique des ligands du CD36." Thèse, 2011. http://hdl.handle.net/1866/8560.

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Les maladies cardiovasculaires sont la principale cause de morbidité et de mortalité dans les pays industrialisés. Le récepteur CD36, exprimé à la surface des macrophages, joue un rôle déterminant dans l’internalisation des lipoprotéines oxydées menant à la formation des cellules spumeuses dans l’espace sous endothélial, première étape du développement des lésions athérosclérotiques. Nous avons montré précédemment que les sécrétines de l’hormone de croissance sont des ligands du récepteur CD36 qui possèdent un site de liaison qui chevauche celui des lipoprotéines oxydées. Cependant, aucune étu

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Carling, Roberta-Daila. "Utilisation d’un modèle de co-culture cellulaire pour l’évaluation in vitro du transport inverse du cholestérol." Thèse, 2012. http://hdl.handle.net/1866/10969.

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Létourneau, Jason. "Les bactéries exprimant AIDA-I interagissent avec l'apolipoprotéine A-I cellulaire." Thèse, 2012. http://hdl.handle.net/1866/9741.

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AIDA-I (adhesin involved in diffuse adherence) est une importante adhésine autotransporteur exprimée par certaines souches de Escherichia. coli impliquée dans la colonisation des porcelets sevrés causant la diarrhée post-sevrage et la maladie de l’œdème. Une précédente étude de notre laboratoire a identifié l’apolipoprotéine AI (ApoAI) du sérum porcin, la protéine structurale des lipoprotéines à haute densité, comme récepteur cellulaire putatif de AIDA-I. L’interaction entre ces deux protéines doit être caractérisée. Ici, nous montrons par ELISA que AIDA-I purifiée est capable d’interagir avec

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