ArticleCell death discovery2025
The role of CARMA3 in regulating fibrosis to prevent hypertrophic cardiomyopathy.
Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- VAP1 promotes cardiac fibrosis by enabling PDGFR signaling in myofibroblasts.Experimental & molecular medicine · 2026Article
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypertrophic cardiomyopathy (HCM) is characterized by cardiac hypertrophy and fibrosis. To investigate the impact of CARMA3 on fibroblast phenotypic transformation in hypertrophic cardiomyopathy (HCM), the correlation between CARMA3 expression and fibrosis was analyzed in HCM patients. Cardiac function and fibroblast phenotypic transformation were assessed in wild-type and CARMA3-knockout mice subjected to transverse aortic constriction (TAC) or angiotensin II treatment. Additionally, cardiac fibroblasts were screened using flow cytometry and proteomic analysis to identify potential targets. Significant cardiac functional impairment and fibrosis were observed in CARMA3-knockout mice following TAC or angiotensin II treatment. Primary fibroblasts isolated from these mice exhibited increased myofibroblast differentiation, extracellular collagen production, mitochondrial damage, and macrophage inflammation. Elevated STAT1 expression was identified in cardiac fibroblasts from CARMA3-knockout mice through proteomic analysis. Additionally, STAT1 phosphorylation was regulated by CARMA3, and an interaction between CARMA3 and STAT1 was detected in response to pressure overload. In conclusion, CARMA3 may suppress myofibroblast activation by inhibiting STAT1 phosphorylation, thereby improving myocardial fibrosis in pressure overload-induced HCM.
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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.