Metabolism of vascular smooth muscle cells in vascular diseases
Abstract
Vascular smooth muscle cells (VSMCs) are the fundamental component of the medial layer of arteries and are essential for arterial physiology and pathology. It is becoming increasingly clear that VSMCs can alter their metabolism to fulfill the bioenergetic and biosynthetic requirements. During vascular injury, VSMCs switch from a quiescent “contractile” phenotype to a highly migratory and proliferative “synthetic” phenotype. Recent studies have found that the phenotype switching of VSMCs is driven by a metabolic switch. Metabolic pathways, including aerobic glycolysis, fatty acid oxidation, and amino acid metabolism, have distinct, indispensable roles in normal and dysfunctional vasculature. VSMCs metabolism is also related to the metabolism of endothelial cells. In the present review, we present a brief overview of VSMCs metabolism and how it regulates the progression of several vascular diseases, including atherosclerosis, systemic hypertension, diabetes, pulmonary hypertension, vascular calcification, and aneurysms, and the effect of the risk factors for vascular disease (aging, cigarette smoking, and excessive alcohol drinking) on VSMC metabolism to clarify the role of VSMCs metabolism in the key pathological process.
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Excessive proliferation of endothelial cells and smooth muscle cells causes intimal hyperplasia, lumen narrowing, local poor blood flow, leading to thrombosis and calcified plaque.
“the excessive proliferation of endothelial cells and smooth muscle cells will cause intimal hyperplasia, lumen narrowing, and local poor blood flow, which will lead to the formation of thrombosis and calcified plaque [162].”
From Application of PLCL as a biodegradable polymer in biomedical engineering (2026) · cites this paper as [162]
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References 283 · Cited by 366
- Authors
- Shi, J., Yang, Y., Cheng, A., Xu, G., & He, F.
- Affiliations
- Tongji Hospital (CN)
- Corresponding author
- He, Fan
- Venue
- American Journal of Physiology-Heart and Circulatory Physiology
- Publisher
- American Physiological Society
- Published
- 2020-09-01
- Volume
- 319
- Issue
- 3
- Pages
- H613-H631
- ISSN
- 0363-6135 (ISSN-L)
- 1522-1539
- OpenAlex
- W3048325813
- Cited by
- 366
- References
- 283
- Citations by year
- 2026: 52 · 2025: 72 · 2024: 103 · 2023: 55 · 2022: 66 · 2021: 16 · 2020: 2
- FWCI
- 3.39
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Journal of Physiology-Heart and Circulatory Physiology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (81974089, 81470948, 81670633)
- international cooperation and exchange projects (81761138041)
- the major research plan of the national natural science foundation of China (91742204)
- the national key research and development program (2016YFC0906103)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
- Keywords
- vascular smooth muscle cells, cellular metabolism, metabolic switch, aerobic glycolysis, fatty acid oxidation, amino acid metabolism, contractile phenotype, synthetic phenotype, vascular injury, atherosclerosis, systemic hypertension, diabetes mellitus, pulmonary hypertension, vascular calcification, aneurysm, endothelial cell metabolism, aging, cigarette smoking, alcohol consumption
- MeSH terms
- Animals, Cell Movement, Energy Metabolism, Humans, Muscle, Smooth, Vascular, Phenotype, Prognosis, Vascular Diseases, Signal Transduction, Cellular Senescence, Myocytes, Smooth Muscle, Cell Proliferation
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