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Research Progress on Histone Deacetylases Regulating Programmed Cell Death in Atherosclerosis

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SPRINGER
DOI: 10.1007/s12265-023-10444-z

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Atherosclerosis; Histone deacetylases; Programmed cell death; Apoptosis; Autophagy; Pyroptosis; Ferroptosis

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This paper provides an overview of the role of histone deacetylases (HDACs) in atherosclerosis and further explores their mechanisms in regulating apoptosis, autophagy, and programmed necrosis. The findings contribute to new measures and theoretical basis for preventing and treating atherosclerosis.
Histone deacetylases (HDACs) are epigenetic modifying enzyme that is closely related to chromatin structure and gene transcription, and numerous studies have found that HDACs play an important regulatory role in atherosclerosis disease. Apoptosis, autophagy and programmed necrosis as the three typical programmed cell death modalities that can lead to cell loss and are closely related to the developmental process of atherosclerosis. In recent years, accumulating evidence has shown that the programmed cell death mediated by HDACs is increasingly important in the pathophysiology of atherosclerosis. This paper first gives a brief overview of HDACs, the mechanism of programmed cell death, and their role in atherosclerosis, and then further elaborates on the role and mechanism of HDACs in regulating apoptosis, autophagy, and programmed necrosis in atherosclerosis, respectively, to provide new effective measures and theoretical basis for the prevention and treatment of atherosclerosis.

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