ReviewFrontiers in cardiovascular medicine2022
Phenotypic plasticity of vascular smooth muscle cells in vascular calcification: Role of mitochondria.
Review in Frontiers in cardiovascular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Urolithin A alleviates vascular remodeling through mitochondrial SIRT3-mediated SOD2 deacetylation and antioxidation in hypertensive rats.Redox report : communications in free radical research · 2026Article
- Sirt1 attenuates calcific aortic valve disease by inhibiting ferroptosis and enhancing mitochondrial function via the activation of the Nrf2/HO‑1/FTH1 axis.International journal of molecular medicine · 2026Article
- Review
- Aldosterone increases the expression and subcellular localization of SERCA2a and SERCA2b in the rat mesenteric artery.Frontiers in physiology · 2026Article
- SIRT1/PGC-1α/Mfn2 pathway regulates mitochondrial homeostasis in VSMC to attenuate aging-related vascular calcification.Scientific reports · 2025Article
- Nanomaterial-induced mitochondrial biogenesis enhances intercellular mitochondrial transfer efficiency.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Phenotypic Switching of VSMCs in the Development of CVDs: Focus on miRs.International journal of molecular sciences · 2025Review
- Review
- Dehydrodiisoeugenol alleviates palmitate-induced mitochondrial dysfunction in human vascular smooth muscle cells through the activation of SIRT1-mediated Drp1 deacetylation.Lipids in health and disease · 2025Article
- Phenotypic switch of vascular smooth muscle cells in COVID-19: Role of cholesterol, calcium, and phosphate.Journal of cellular physiology · 2024Review
- Mitochondrial Dysfunction as a Potential Mechanism Mediating Cardiac Comorbidities in Parkinson's Disease.International journal of molecular sciences · 2024Review
- A Modified Protocol for the Isolation, Culture, and Characterization of Human Smooth Muscle Cells from the Umbilical Cord.Methods and protocols · 2023Article
- Biological function, mediate cell death pathway and their potential regulated mechanisms for post-mortem muscle tenderization of PARP1: A review.Frontiers in nutrition · 2022Review
- Dietary Salt Can Be Crucial for Food-Induced Vascular Inflammation.Clinical pathology (Thousand Oaks, Ventura County, Calif.)Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vascular calcification (VC) is an important hallmark of cardiovascular disease, the osteo-/chondrocyte phenotype differentiation of vascular smooth muscle cells (VSMCs) is the main cause of vascular calcification. Accumulating evidence shows that mitochondrial dysfunction may ultimately be more detrimental in the VSMCs calcification. Mitochondrial participate in essential cellular functions, including energy production, metabolism, redox homeostasis regulation, intracellular calcium homeostasis, apoptosis, and signal transduction. Mitochondrial dysfunction under pathological conditions results in mitochondrial reactive oxygen species (ROS) generation and metabolic disorders, which further lead to abnormal phenotypic differentiation of VSMCs. In this review, we summarize existing studies targeting mitochondria as a treatment for VC, and focus on VSMCs, highlighting recent progress in determining the roles of mitochondrial processes in regulating the phenotype transition of VSMCs, including mitochondrial biogenesis, mitochondrial dynamics, mitophagy, mitochondrial energy metabolism, and mitochondria/ER interactions. Along these lines, the impact of mitochondrial homeostasis on VC is discussed.
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