ArticleAntioxidants & redox signaling2019
Transient Receptor Potential Canonical 3 and Nuclear Factor of Activated T Cells C3 Signaling Pathway Critically Regulates Myocardial Fibrosis.
Article in Antioxidants & redox signaling, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
13 citing papers in PubMed, 18 citations in OpenAlex.
- CaBiomedicines · 2025Review
- Inhibiting atrial natriuretic peptide clearance reduces myocardial fibrosis and improves cardiac function in diabetic rats.European heart journal open · 2025Article
- TRPC3 contributes to cyclophosphamide-induced cystitis progression by enhancing bladder fibrosis through activation of the TGF-β/smad pathway.Frontiers in pharmacology · 2025Article
- Canonical transient receptor potential channel 1 aggravates myocardial ischemia-and-reperfusion injury by upregulating reactive oxygen species.Journal of pharmaceutical analysis · 2023Article
- TRPC3 Regulates Islet Beta-Cell Insulin Secretion.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Progress on role of ion channels of cardiac fibroblasts in fibrosis.Frontiers in physiology · 2023Review
- FAM114A1 influences cardiac pathological remodeling by regulating angiotensin II signaling.JCI insight · 2022Article
- Emerging role of transient receptor potential (TRP) ion channels in cardiac fibroblast pathophysiology.Frontiers in physiology · 2022Review
- Angiotensin-II-Evoked CaCells · 2020Article
- TRPC Channels: Dysregulation and CaCells · 2020Review
- Differential Gender-Dependent Patterns of Cardiac Fibrosis and Fibroblast Phenotypes in Aging Mice.Oxidative medicine and cellular longevity · 2020Article
- The Pivotal Role of TRP Channels in Homeostasis and Diseases throughout the Gastrointestinal Tract.International journal of molecular sciences · 2019Review
- Upregulation of Transient Receptor Potential Canonical Type 3 Channel via AT1R/TGF-Oxidative medicine and cellular longevity · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
Abstract
aimsCardiac fibroblasts (CFs) are emerging as major contributors to myocardial fibrosis (MF), a final common pathway of many etiologies of heart disease. Here, we studied the functional relevance of transient receptor potential canonical 3 (TRPC3) channels and nuclear factor of activated T cells c3 (NFATc3) signaling in rodent and human ventricular CFs, and whether their modulation would limit MF.
resultsA positive feedback loop between TRPC3 and NFATc3 drove a rat ventricular CF fibrotic phenotype. In these cells, polyphenols (extract of grape pomace polyphenol [P.E.]) decreased basal and angiotensin II-mediated Ca
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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.