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Published on: November 30, 2018
Research Progress on Histone Deacetylases Regulating Programmed Cell Death in Atherosclerosis
Gang Zhou1,2,3, Yanfang Liu1,2,3, Hui Wu4,5,6
1Institute of Cardiovascular Disease, China Three Gorges University, Yichang, 443003, China.
Insights
Histone deacetylases (HDACs) regulate programmed cell death pathways like apoptosis and autophagy, which are crucial in atherosclerosis development. Understanding HDACs offers new therapeutic targets for this cardiovascular disease.
Area of Science:
- Epigenetics
- Molecular Biology
- Cardiovascular Disease Research
Background:
- Histone deacetylases (HDACs) are epigenetic enzymes influencing gene transcription and chromatin structure.
- HDACs play a significant role in the pathophysiology of atherosclerosis.
- Programmed cell death, including apoptosis, autophagy, and programmed necrosis, is implicated in atherosclerosis progression.
Purpose of the Study:
- To provide an overview of HDACs and programmed cell death mechanisms.
- To elaborate on the specific roles of HDACs in regulating apoptosis, autophagy, and programmed necrosis in atherosclerosis.
- To offer a theoretical basis for novel therapeutic strategies against atherosclerosis.
Main Methods:
- Review of existing literature on HDACs, programmed cell death, and atherosclerosis.
- Analysis of the molecular mechanisms by which HDACs modulate apoptosis, autophagy, and programmed necrosis.
- Synthesis of current evidence to highlight the therapeutic potential of targeting HDACs.
Main Results:
- HDACs are key regulators of multiple programmed cell death pathways relevant to atherosclerosis.
- Specific HDACs influence apoptosis, autophagy, and programmed necrosis in the context of atherosclerotic disease.
- Targeting HDACs presents a promising avenue for managing atherosclerosis.
Conclusions:
- HDACs are critical mediators in the programmed cell death processes underlying atherosclerosis.
- Further research into HDAC-mediated cell death mechanisms can inform the development of targeted therapies.
- Modulating HDAC activity holds potential for preventing and treating atherosclerosis.
Abstract:
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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