Atherogenic Dyslipidemia After Liver Transplantation: Mechanisms and Clinical Implications

Cardiovascular disease (CVD), particularly atherosclerosis‐associated CVD, is a major cause of long‐term mortality after liver transplantation (LT). The liver is central in lipid homeostasis, and changes associated with insulin resistance, weight gain, adipose tissue inflammation, and development of...

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Veröffentlicht in:Liver transplantation 2021-09, Vol.27 (9), p.1326-1333
Hauptverfasser: Syed, Taseen, Siddiqui, Mohammad S.
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container_title Liver transplantation
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creator Syed, Taseen
Siddiqui, Mohammad S.
description Cardiovascular disease (CVD), particularly atherosclerosis‐associated CVD, is a major cause of long‐term mortality after liver transplantation (LT). The liver is central in lipid homeostasis, and changes associated with insulin resistance, weight gain, adipose tissue inflammation, and development of nonalcoholic fatty liver disease (NAFLD) after LT promote atherogenesis. These factors synergistically alter lipid homeostasis, thereby leading to the production of proatherogenic lipoproteins, which contribute to the heighted risk of CVD‐associated events observed in LT recipients. Although the exact mechanism promoting this shift of a proatherogenic lipoprotein profile is currently not known, the choice of immunosuppression and preexisting metabolic risk factors (ie, NAFLD) are likely contributors. This shift in proatherogenic lipoprotein subparticles presents clinical challenges as the traditional lipid profile employed in clinical practice may not fully capture this atherogenic risk. This review focuses on lipoprotein metabolism and atherogenesis in LT recipients. https://wileyhealthlearning.com/#/online-courses/ddb74a8d-493b-4e33-b8cc-820c79cff7cc
doi_str_mv 10.1002/lt.26069
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The liver is central in lipid homeostasis, and changes associated with insulin resistance, weight gain, adipose tissue inflammation, and development of nonalcoholic fatty liver disease (NAFLD) after LT promote atherogenesis. These factors synergistically alter lipid homeostasis, thereby leading to the production of proatherogenic lipoproteins, which contribute to the heighted risk of CVD‐associated events observed in LT recipients. Although the exact mechanism promoting this shift of a proatherogenic lipoprotein profile is currently not known, the choice of immunosuppression and preexisting metabolic risk factors (ie, NAFLD) are likely contributors. This shift in proatherogenic lipoprotein subparticles presents clinical challenges as the traditional lipid profile employed in clinical practice may not fully capture this atherogenic risk. 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subjects Adipose tissue
Arteriosclerosis
Atherogenesis
Cardiovascular diseases
Dyslipidemia
Fatty liver
Homeostasis
Immunosuppression
Insulin
Insulin resistance
Lipid metabolism
Lipids
Lipoproteins
Liver
Liver diseases
Liver transplantation
Liver transplants
Metabolic disorders
Risk factors
title Atherogenic Dyslipidemia After Liver Transplantation: Mechanisms and Clinical Implications
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