ArticleScientific reports2022
p38 MAPK priming boosts VSMC proliferation and arteriogenesis by promoting PGC1α-dependent mitochondrial dynamics.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 14 citations in OpenAlex.
- Dieckol suppresses lipid accumulation and promotes thermogenic markers in 3T3-L1 adipocytes via ERK/p38 MAPK signaling.Journal of physiology and biochemistry · 2026Article
- Bioactive Constituents and Therapeutic Mechanisms of Shenfu Decoction in a Rat Model of Seawater-Immersion-Induced Accidental Hypothermia.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Corilagin inhibits the proliferation of vascular smooth muscle and excessive matrix deposition following vascular injury via the MAPK pathway.Journal of muscle research and cell motility · 2025Article
- How Can Molecules Induce Hemorrhoids? The Role of Genetics and Epigenetics in Hemorrhoidal Disease.International journal of molecular sciences · 2025Review
- Targeting Mitochondrial Reactive Oxygen Species: JP4-039's Potential as a Cardiovascular Therapeutic.Journal of clinical medicine · 2025Review
- PGC-1α Regulates Exercise Intensity-Dependent Atrial Remodeling and Fibrillation in Rats.Aging and disease · 2025Article
- Investigation of the mechanism of hypertension caused by BTKi in the treatment of hematologic diseases.Frontiers in pharmacology · 2025Review
- Synthetic Antiangiogenic Vascular Endothelial Growth Factor-A Splice Variant Revascularizes Ischemic Muscle in Peripheral Artery Disease.Journal of the American Heart Association · 2024Article
- Article
- Molecular Mechanisms Driven by MT4-MMP in Cancer Progression.International journal of molecular sciences · 2023Review
- Identification of the microRNA alterations in extracellular vesicles derived from human haemorrhoids.Experimental physiology · 2023Article
- Mitochondrial dynamics in vascular remodeling and target-organ damage.Frontiers in cardiovascular medicine · 2023Review
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vascular smooth muscle cell (VSMC) proliferation is essential for arteriogenesis to restore blood flow after artery occlusion, but the mechanisms underlying this response remain unclear. Based on our previous findings showing increased VSMC proliferation in the neonatal aorta of mice lacking the protease MT4-MMP, we aimed at discovering new players in this process. We demonstrate that MT4-MMP absence boosted VSMC proliferation in vitro in response to PDGF-BB in a cell-autonomous manner through enhanced p38 MAPK activity. Increased phospho-p38 in basal MT4-MMP-null VSMCs augmented the rate of mitochondrial degradation by promoting mitochondrial morphological changes through the co-activator PGC1α as demonstrated in PGC1α
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