ArticleArteriosclerosis, thrombosis, and vascular biology2015
Myocardin regulates vascular smooth muscle cell inflammatory activation and disease.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers, 1 of them a synthesis that pooled it.
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Who cites it
76 citing papers in PubMed, 1 synthesis or guideline pooled it, 137 citations in OpenAlex.
- Twenty-Five Novel Loci for Carotid Intima-Media Thickness: A Genome-Wide Association Study in >45 000 Individuals and Meta-Analysis of >100 000 Individuals.Arteriosclerosis, thrombosis, and vascular biology · 2022Pooled it
- Myeloid Ecotropic Viral Integration Site 1 Promotes Vascular Smooth Muscle Differentiation through Activation of Myocardin.bioRxiv : the preprint server for biology · 2026Article
- Spatial expression of myocardin protein in normal and disease states.American journal of physiology. Cell physiology · 2026Article
- Review
- Genetic silencing of KChannels (Austin, Tex.) · 2025Article
- YAP/TAZ deletion in vascular smooth muscle cells mirrors atherosclerosis-associated transcriptional programs.Journal of molecular and cellular cardiology plus · 2025Article
- Mapping atherogenesis mechanisms in smooth muscle cells by targeting genes linked to coronary artery disease.iScience · 2025Article
- C-Kit Is Essential for Vascular Smooth Muscle Cell Phenotypic Switch In Vitro and In Vivo After Injury.Cells · 2025Article
- Premature cell senescence promotes vascular smooth muscle cell phenotypic modulation and resistance to re-differentiation.Cardiovascular research · 2025Article
- Interleukin-1 Signaling on Vascular Smooth Muscle Cells Accelerates Atherosclerosis in a Murine Model of Kawasaki Disease.Journal of the American Heart Association · 2025Article
- YBX1 Modulates Intimal Hyperplasia by Regulating Expression and Alternative Splicing of Cell Cycle Associated Genes in RASMCs.Journal of cellular and molecular medicine · 2025Article
- Mechanisms of AGE-induced VSMC phenotypic switching and macrophage modulation in human abdominal aortic aneurysms.Experimental biology and medicine (Maywood, N.J.) · 2025Article
- Exploration of potential biomarkers and immune cell infiltration characteristics for peripheral atherosclerosis in sjögren's syndrome based on comprehensive bioinformatics analysis and machine learning.Frontiers in genetics · 2025Article
- Role of long noncoding RNAs in diabetes-associated peripheral arterial disease.Cardiovascular diabetology · 2024Review
- Suppression of smooth muscle cell inflammation by myocardin-related transcription factors involves inactivation of TANK-binding kinase 1.Scientific reports · 2024Article
- Triglyceride-rich lipoproteins and cardiovascular diseases.Frontiers in endocrinology · 2024Review
- Interstitial Fluid Shear Stress Induces the Synthetic Phenotype Switching of VSMCs to Release Pro-calcified Extracellular Vesicles via EGFR-MAPK-KLF5 Pathway.International journal of biological sciences · 2024Article
- Mechanistic insights into the regression of atherosclerotic plaques.Frontiers in physiology · 2024Review
- Vascular smooth muscle-specific YAP/TAZ deletion triggers aneurysm development in mouse aorta.JCI insight · 2023Article
- SMYD2 regulates vascular smooth muscle cell phenotypic switching and intimal hyperplasia via interaction with myocardin.Cellular and molecular life sciences : CMLS · 2023Article
16 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 1 institution in 2 countries.
Funding
Abstract
objectiveAtherosclerosis, the cause of 50% of deaths in westernized societies, is widely regarded as a chronic vascular inflammatory disease. Vascular smooth muscle cell (VSMC) inflammatory activation in response to local proinflammatory stimuli contributes to disease progression and is a pervasive feature in developing atherosclerotic plaques. Therefore, it is of considerable therapeutic importance to identify mechanisms that regulate the VSMC inflammatory response. APPROACH AND
resultsWe report that myocardin, a powerful myogenic transcriptional coactivator, negatively regulates VSMC inflammatory activation and vascular disease. Myocardin levels are reduced during atherosclerosis, in association with phenotypic switching of smooth muscle cells. Myocardin deficiency accelerates atherogenesis in hypercholesterolemic apolipoprotein E(-/-) mice. Conversely, increased myocardin expression potently abrogates the induction of an array of inflammatory cytokines, chemokines, and adhesion molecules in VSMCs. Expression of myocardin in VSMCs reduces lipid uptake, macrophage interaction, chemotaxis, and macrophage-endothelial tethering in vitro, and attenuates monocyte accumulation within developing lesions in vivo. These results demonstrate that endogenous levels of myocardin are a critical regulator of vessel inflammation.
conclusionsWe propose myocardin as a guardian of the contractile, noninflammatory VSMC phenotype, with loss of myocardin representing a critical permissive step in the process of phenotypic transition and inflammatory activation, at the onset of vascular disease.
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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.