LncRNA-modulated autophagy in plaque cells: a new paradigm of gene regulation in atherosclerosis?
| Autor: | Kun Ren, Qi-Xian Liu, Meng-Qi Li, Xi-Long Zheng, Xiao-Dan Xu, Meng-Wen Shi, Kai Yin, Guo-Jun Zhao, Ting Jiang, Xiao-Hai Yu |
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| Rok vydání: | 2020 |
| Předmět: |
autophagy
Aging Vascular smooth muscle Autophagy-Related Proteins Inflammation Review Cell fate determination Animals Humans Medicine long noncoding RNAs Cell damage Cell Proliferation Regulation of gene expression business.industry Macrophages Autophagy Arteries Cell Biology Atherosclerosis medicine.disease Plaque Atherosclerotic Cell biology Gene Expression Regulation Apoptosis Cytoplasm RNA Long Noncoding Inflammation Mediators medicine.symptom business Signal Transduction |
| Zdroj: | Aging (Albany NY) |
| ISSN: | 1945-4589 |
| DOI: | 10.18632/aging.103786 |
| Popis: | The development of atherosclerosis is accompanied by the functional deterioration of plaque cells, which leads to the escalation of endothelial inflammation, abnormal vascular smooth muscle cell phenotype switching and the accumulation of lipid-laden macrophages within vascular walls. Autophagy, a highly conserved homeostatic mechanism, is critical for the delivery of cytoplasmic substrates to lysosomes for degradation. Moderate levels of autophagy prevent atherosclerosis by safeguarding plaque cells against apoptosis, preventing inflammation, and limiting the lipid burden, whereas excessive autophagy exacerbates cell damage and inflammation and thereby accelerates the formation of atherosclerotic plaques. Increasing lines of evidence suggest that long noncoding RNAs can be either beneficial or detrimental to atherosclerosis development by regulating the autophagy level. This review summarizes the research progress related to 1) the significant role of autophagy in atherosclerosis and 2) the effects of the lncRNA-mediated modulation of autophagy on the plaque cell fate, inflammation levels, proliferative capacity, and cholesterol metabolism and subsequently on atherogenesis. |
| Databáze: | OpenAIRE |
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