ArticleCell death & disease2018
COMP-prohibitin 2 interaction maintains mitochondrial homeostasis and controls smooth muscle cell identity.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 32 citations in OpenAlex.
- Energetic Decoding of VSMC Plasticity: Metabolic Reprogramming and Phenotypic Switching.Cardiovascular drugs and therapy · 2026Review
- Topical vascular organoid therapy promotes microvascular regeneration and functional recovery in porcine ischemic cardiomyopathy.Stem cell reports · 2026Article
- Aligned core-sheath structured fibers prevent intimal hyperplasia via modulate macrophage polarization and smooth muscle cell phenotype in vascular regeneration.Journal of nanobiotechnology · 2026Article
- Age and Sex Impact the Role of Thrombospondin-2 and Thrombospondin-5 in Response to Hindlimb Ischemia.FASEB bioAdvances · 2026Article
- FAM177A1 disrupts SIRT3-SOD2 signaling to drive mitochondrial dysfunction-mediated VSMC phenotypic switching in vascular remodeling.International journal of biological sciences · 2026Article
- Irisin targets the HK1-glycolysis-NLRP3 pyroptosis axis to prevent chronic kidney disease-associated vascular calcification.Renal failure · 2025Article
- PKM2 crotonylation reprograms glycolysis in VSMCs, contributing to phenotypic switching.Oncogene · 2025Article
- Extracellular matrix in vascular homeostasis and disease.Nature reviews. Cardiology · 2025Review
- Affinity-Enriched Plasma Proteomics for Biomarker Discovery in Abdominal Aortic Aneurysms.Proteomes · 2024Article
- The molecular mechanism of thrombospondin family members in cardiovascular diseases.Frontiers in cardiovascular medicine · 2024Review
- Mitophagy in atherosclerosis: from mechanism to therapy.Frontiers in immunology · 2023Review
- Research progress on the mechanism of phenotypic transformation of pulmonary artery smooth muscle cells induced by hypoxia.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2022Review
- Endothelin-1 depletion of cartilage oligomeric matrix protein modulates pulmonary artery superoxide and iron metabolism-associated mitochondrial heme biosynthesis.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- Phenotypic plasticity of vascular smooth muscle cells in vascular calcification: Role of mitochondria.Frontiers in cardiovascular medicine · 2022Review
- Mitochondrial Dysfunction: Cause or Consequence of Vascular Calcification?Frontiers in cell and developmental biology · 2021Review
- Cell Death Signaling Pathway Induced by Cholix Toxin, a Cytotoxin and eEF2 ADP-Ribosyltransferase Produced byToxins · 2020Review
- Extracellular matrix dynamics in vascular remodeling.American journal of physiology. Cell physiology · 2020Review
- Impact of β-glycerophosphate on the bioenergetic profile of vascular smooth muscle cells.Journal of molecular medicine (Berlin, Germany) · 2020Article
- Hypermethylation of mitochondrial DNA in vascular smooth muscle cells impairs cell contractility.Cell death & disease · 2020Article
- Metformin and Vascular Diseases: A Focused Review on Smooth Muscle Cell Function.Frontiers in pharmacology · 2020Review
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vascular smooth muscle cells (VSMCs) are highly phenotypically plastic, and loss of the contractile phenotype in VSMCs has been recognized at the early onset of the pathology of a variety of vascular diseases. However, the endogenous regulatory mechanism to maintain contractile phenotype in VSMCs remains elusive. Moreover, little has been known about the role of the mitochondrial bioenergetics in terms of VSMC homeostasis. Herein, we asked if glycoprotein COMP (Cartilage oligomeric matrix protein) is involved in mitochondrial bioenergetics and therefore regulates VSMCs homeostasis. By using fluorescence assay, subcellular western blot and liquid chromatography tandem mass spectrometry analysis, we found that extracellular matrix protein COMP unexpectedly localized within mitochondria. Further mitochondrial transplantation revealed that both mitochondrial and non-mitochondrial COMP maintained VSMC identity. Moreover, microarray analysis revealed that COMP deficiency impaired mitochondrial oxidative phosphorylation in VSMCs. Further study confirmed that COMP deficiency caused mitochondrial oxidative phosphorylation dysfunction accompanied by morphological abnormality. Moreover, the interactome of mitochondrial COMP revealed that COMP interacted with prohibitin 2, and COMP-prohibitin 2 interaction maintained mitochondrial homeostasis. Additionally, disruption of COMP-prohibitin 2 interaction caused VSMC dedifferentiation in vitro and enhanced the neointima formation post rat carotid artery injury in vivo. In conclusion, COMP-prohibitin 2 interaction in mitochondria plays an important role in maintaining the contractile phenotype of VSMCs by regulating mitochondrial oxidative phosphorylation. Maintaining the homeostasis of mitochondrial respiration through COMP-prohibitin 2 interaction may shed light on prevention of vascular disease.
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