CD36, also known as the scavenger receptor B2, is a
multifunctional receptor widely expressed in various organs. CD36 is expressed
in various tissues, including endothelial cells, cardiac muscle cells, renal
tubular epithelial cells, liver cells, adipocytes, platelets, and macrophages,
and is involved in many pathophysiological processes, including immune
regulation and metabolic regulation. CD36 plays a crucial role in the uptake of
long-chain fatty acids, the main metabolic substrate in myocardial tissue. The
maturation and transportation of CD36 is regulated by post-translational
modifications, including phosphorylation, ubiquitination, glycosylation, and
palmitoylation. CD36 is decreased in pathological cardiac hypertrophy caused by
ischaemia–reperfusion and pressure overload, and increased in diabetic
cardiomyopathy and atherosclerosis. Deficiency of CD36 alleviates diabetic
cardiomyopathy and atherosclerosis, while overexpression of CD36 eliminates
ischaemia–reperfusion damage, together suggesting that CD36 is closely
associated with the progression of cardiovascular diseases and may be a new
therapeutic target. Transcriptional activation, post-translational
modification, and localization changes of CD36 may provide new directions for
the treatment of cardiovascular diseases. This review summarizes the regulation
and post-translational modifications of CD36 and evaluates its role in
cardiovascular diseases and its potential as a therapeutic target.
Author(s) Details:
Hongyang Shu,
Division of Cardiology, Department of Internal Medicine, Tongji
Hospital, Tongji Medical College, Huazhong University of Science and Technology,
Wuhan-430000, China and Hubei Key Laboratory of Genetics and Molecular
Mechanism of Cardiologic Disorders, Huazhong University of Science and
Technology, Wuhan-430000, China.
Yizhong
Peng,
Department
of Orthopedics, Union Hospital, Tongji Medical College, Huazhong University of
Science and Technology, Wuhan-430000, China.
Weijian Hang,
Division of Cardiology, Department of Internal Medicine, Tongji
Hospital, Tongji Medical College, Huazhong University of Science and
Technology, Wuhan-430000, China and Hubei Key Laboratory of Genetics and
Molecular Mechanism of Cardiologic Disorders, Huazhong University of Science
and Technology, Wuhan-430000, China.
Jiali Nie,
Division of Cardiology, Department of Internal Medicine, Tongji
Hospital, Tongji Medical College, Huazhong University of Science and
Technology, Wuhan-430000, China and Hubei Key Laboratory of Genetics and
Molecular Mechanism of Cardiologic Disorders, Huazhong University of Science
and Technology, Wuhan-430000, China.
Ning Zhou,
Division
of Cardiology, Department of Internal Medicine, Tongji Hospital, Tongji Medical
College, Huazhong University of Science and Technology, Wuhan-430000, China and
Hubei Key Laboratory of Genetics and Molecular Mechanism of Cardiologic
Disorders, Huazhong University of Science and Technology, Wuhan-430000, China.
Dao
Wen Wang,
Division
of Cardiology, Department of Internal Medicine, Tongji Hospital, Tongji Medical
College, Huazhong University of Science and Technology, Wuhan-430000, China and
Hubei Key Laboratory of Genetics and Molecular Mechanism of Cardiologic
Disorders, Huazhong University of Science and Technology, Wuhan-430000, China.
Please see the link here: https://stm.bookpi.org/RUDHR-V3/article/view/13548
