ReviewInternational journal of molecular sciences2023
Mitochondrial Homeostasis in VSMCs as a Central Hub in Vascular Remodeling.
Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
42 citing papers in PubMed, 58 citations in OpenAlex.
- Mitochondrial Fusion and Fission in Age-Related Cardio-Cerebral Diseases: Mechanisms and Interventions.Aging cell · 2026Review
- Smooth Muscle Cell Plasticity as a Central Determinant of Plaque Stability.Current atherosclerosis reports · 2026Review
- ZHX2 Alleviates Vascular Remodeling and Smooth Muscle Cell Proliferation by Transcriptional Regulation of GADD45G.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Neointimal hyperplasia and vascular restenosis: from molecular mechanisms to therapeutic interventions.Molecular biomedicine · 2026Review
- Article
- PDK4 drives abdominal aortic aneurysm by promoting smooth muscle cell metabolic reprogramming and NLRP3-mediated pyroptosis.Nature communications · 2026Article
- Mitochondrial cardiovascular diseases: molecular mechanisms, multi-omics exploration and therapeutic strategies.Journal of advanced research · 2026Review
- Integrating machine learning and multi-omics analysis to explore Treg-associated programmed cell death features in clear cell renal cell carcinoma.Cancer cell international · 2026Article
- Role and mechanisms of vascular smooth muscle cell phenotypic transition in diabetic macrovascular complications.Biological research · 2026Review
- Therapeutic Implication of Anti-CTGF in Neointimal Hyperplasia via Regulating Mitochondrial Dysfunction and VSMC Phenotypic Switch.Cardiovascular therapeutics · 2026Article
- SPARC modulates macrophage-like phenotype transformation in VSMCs and triggers a vicious cycle.Frontiers in cell and developmental biology · 2026Article
- Unveiling Heart Failure: Gender-Specific Insights and Innovations in Women's Cardiac Health.Current pharmaceutical design · 2026Review
- Mitochondrial dysfunction in aortic aneurysm and dissection: mechanisms and therapeutic implications.Frontiers in pharmacology · 2026Review
- Mechanisms and treatment modalities related to premature ovarian insufficiency in mitochondria: literature review.Journal of ovarian research · 2025Review
- Reprogramming the Mitochondrion in Atherosclerosis: Targets for Vascular Protection.Antioxidants (Basel, Switzerland) · 2025Review
- 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
- Mitochondrial Transport Proteins in Cardiovascular Diseases: Metabolic Gatekeepers, Pathogenic Mediators and Therapeutic Targets.International journal of molecular sciences · 2025Review
- How to measure and model cardiovascular aging.Cardiovascular research · 2025Review
- Multidimensional excavation of the current status and trends of mechanobiology in cardiovascular homeostasis and remodeling within 20 years.Mechanobiology in medicine · 2025Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Vascular remodeling is a common pathological hallmark of many cardiovascular diseases. Vascular smooth muscle cells (VSMCs) are the predominant cell type lining the tunica media and play a crucial role in maintaining aortic morphology, integrity, contraction and elasticity. Their abnormal proliferation, migration, apoptosis and other activities are tightly associated with a spectrum of structural and functional alterations in blood vessels. Emerging evidence suggests that mitochondria, the energy center of VSMCs, participate in vascular remodeling through multiple mechanisms. For example, peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α)-mediated mitochondrial biogenesis prevents VSMCs from proliferation and senescence. The imbalance between mitochondrial fusion and fission controls the abnormal proliferation, migration and phenotypic transformation of VSMCs. Guanosine triphosphate-hydrolyzing enzymes, including mitofusin 1 (MFN1), mitofusin 2 (MFN2), optic atrophy protein 1 (OPA1) and dynamin-related protein 1 (DRP1), are crucial for mitochondrial fusion and fission. In addition, abnormal mitophagy accelerates the senescence and apoptosis of VSMCs. PINK/Parkin and NIX/BINP3 pathways alleviate vascular remodeling by awakening mitophagy in VSMCs. Mitochondrial DNA (mtDNA) damage destroys the respiratory chain of VSMCs, resulting in excessive ROS production and decreased ATP levels, which are related to the proliferation, migration and apoptosis of VSMCs. Thus, maintaining mitochondrial homeostasis in VSMCs is a possible way to relieve pathologic vascular remodeling. This review aims to provide an overview of the role of mitochondria homeostasis in VSMCs during vascular remodeling and potential mitochondria-targeted therapies.
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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.