ArticleRedox biology2013
Mitochondrial fission induced by platelet-derived growth factor regulates vascular smooth muscle cell bioenergetics and cell proliferation.
Article in Redox biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
102 citing papers in PubMed, 165 citations in OpenAlex.
- Article
- Cholesterol-driven mitochondrial rejuvenation by quercetin nanotherapeutics restores implant osseointegration in diabetes.Bioactive materials · 2026Article
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- Nitrite increases mitofusin-1 levels to inhibit vascular smooth muscle cell proliferation and prevent intimal hyperplasia.Redox biology · 2026Article
- Lactylation and lactate: insights into muscle cell epigenetic regulators in exercise.Molecular medicine (Cambridge, Mass.) · 2026Review
- RIMKLA promotes hypertension by activating PKM2 to trigger VSMC phenotype switch.Military Medical Research · 2026Article
- Association between free fatty acids and vascular calcification in CKD patients.Frontiers in physiology · 2026Article
- Vascular smooth muscle cell metabolic reprogramming and phenotypic remodeling in atherosclerosis.Cell death discovery · 2025Review
- Leptin Aggravates Thoracic Aortic Dissection Through Impairment of Energy Metabolism in Nrip2Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Review
- Pyruvate kinase splice variants in fibroblasts influence cardiac remodeling after myocardial infarction in male mice.Journal of molecular and cellular cardiology · 2025Article
- The Pathophysiological Role of Vascular Smooth Muscle Cells in Abdominal Aortic Aneurysm.Cells · 2025Review
- PKM2 crotonylation reprograms glycolysis in VSMCs, contributing to phenotypic switching.Oncogene · 2025Article
- Mitochondrial quality control as a therapeutic target in cardiovascular disease: Mechanistic insights and future directions.Journal of translational internal medicine · 2025Article
- Platelet Extracellular Vesicles as Natural Delivery Vehicles for Mitochondrial Dysfunction Therapy?ACS biomaterials science & engineering · 2025Review
- Lactate Dehydrogenase A Crotonylation and Mono-Ubiquitination Maintains Vascular Smooth Muscle Cell Growth and Migration and Promotes Neointima Hyperplasia.Journal of the American Heart Association · 2025Article
- Dysregulation of Mitochondrial Homeostasis in Cardiovascular Diseases.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Mechanical Activation of cPLA2 Impedes Fatty Acid β-Oxidation in Vein Grafts.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Dynamic regulation of neutrophil immunometabolism by platelet-derived metabolites.Frontiers in immunology · 2025Review
- Mitochondrial DNA in atherosclerosis research progress: a mini review.Frontiers in immunology · 2025Review
42 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Vascular smooth muscle cells (VSMCs) develop a highly proliferative and synthetic phenotype in arterial diseases. Because such phenotypic changes are likely integrated with the energetic state of the cell, we hypothesized that changes in cellular metabolism regulate VSMC plasticity. VSMCs were exposed to platelet-derived growth factor-BB (PDGF) and changes in mitochondrial morphology, proliferation, contractile protein expression, and mitochondrial metabolism were examined. Exposure of VSMCs to PDGF resulted in mitochondrial fragmentation and a 50% decrease in the abundance of mitofusin 2. Synthetic VSMCs demonstrated a 20% decrease in glucose oxidation, which was accompanied by an increase in fatty acid oxidation. Results of mitochondrial function assays in permeabilized cells showed few changes due to PDGF treatment in mitochondrial respiratory chain capacity and coupling. Treatment of VSMCs with Mdivi-1-an inhibitor of mitochondrial fission-inhibited PDGF-induced mitochondrial fragmentation by 50% and abolished increases in cell proliferation; however, it failed to prevent PDGF-mediated activation of autophagy and removal of contractile proteins. In addition, treatment with Mdivi-1 reversed changes in fatty acid and glucose oxidation associated with the synthetic phenotype. These results suggest that changes in mitochondrial morphology and bioenergetics underlie the hyperproliferative features of the synthetic VSMC phenotype, but do not affect the degradation of contractile proteins. Mitochondrial fragmentation occurring during the transition to the synthetic phenotype could be a therapeutic target for hyperproliferative vascular disorders.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.