ArticleAmerican journal of physiology. Heart and circulatory physiology2012
Cardiomyocyte ATP release through pannexin 1 aids in early fibroblast activation.
Article in American journal of physiology. Heart and circulatory physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
What it found
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Who cites it
64 citing papers in PubMed, 106 citations in OpenAlex.
- Review
- Multiple triggering mechanisms of myocardial fibrosis: Comparison and integration in different disease contexts.iScience · 2026Review
- Pannexins in the heart: cell-specific expression and contributions to disease.Cell and tissue research · 2026Review
- Pannexins in the vasculature.American journal of physiology. Heart and circulatory physiology · 2025Review
- Pannexin1 via P2rx7/amphiregulin contributes to cardiac fibrosis post myocardial infarction.Journal of molecular histology · 2025Article
- Proximal tubule pannexin 1 contributes to mitochondrial dysfunction and cell death during acute kidney injury.American journal of physiology. Renal physiology · 2025Article
- The impact of Panx1 on inflammation, immunity, and cancer: a comprehensive review.Frontiers in medicine · 2025Review
- Molecular and metabolic landscape of adenosine triphosphate-induced cell death in cardiovascular disease.World journal of cardiology · 2024Review
- Cardiomyocyte PANX1 Controls Glycolysis and Neutrophil Recruitment in Hypertrophy.Circulation research · 2024Article
- Pannexin 1 dysregulation in Duchenne muscular dystrophy and its exacerbation of dystrophic features in mdx mice.Skeletal muscle · 2024Article
- ATP releasing channels and the ameliorative effects of high intensity interval training on diabetic heart: a multifaceted analysis.Scientific reports · 2024Article
- Cardiomyocyte intercellular signalling increases oxidative stress and reprograms the global- and phospho-proteome of cardiac fibroblasts.Journal of extracellular biology · 2023Article
- Vascular Endothelial Barrier Protection Prevents Atrial Fibrillation by Preserving Cardiac Nanostructure.JACC. Clinical electrophysiology · 2023Article
- Role of cAMP in Cardiomyocyte Viability: Beneficial or Detrimental?Circulation research · 2023Article
- Mitochondrial pannexin1 controls cardiac sensitivity to ischaemia/reperfusion injury.Cardiovascular research · 2023Article
- Connexin 37, 40, 43 and Pannexin 1 Expression in the Gastric Mucosa of Patients with Systemic Sclerosis.Biomedicines · 2023Article
- Article
- Hydrogel delivery of purinergic enzymes improves cardiac ischemia/reperfusion injury.Journal of molecular and cellular cardiology · 2023Article
- The Pleiotropic Role of Extracellular ATP in Myocardial Remodelling.Molecules (Basel, Switzerland) · 2023Review
- The ATP-dependent Pathways and Human Diseases.Current medicinal chemistry · 2023Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
Abstract
Fibrosis following myocardial infarction is associated with increases in arrhythmias and sudden cardiac death. Initial steps in the development of fibrosis are not clear; however, it is likely that cardiac fibroblasts play an important role. In immune cells, ATP release from pannexin 1 (Panx1) channels acts as a paracrine signal initiating activation of innate immunity. ATP has been shown in noncardiac systems to initiate fibroblast activation. Therefore, we propose that ATP release through Panx1 channels and subsequent fibroblast activation in the heart drives the development of fibrosis in the heart following myocardial infarction. We identified for the first time that Panx1 is localized within sarcolemmal membranes of canine cardiac myocytes where it directly interacts with the postsynaptic density 95/Drosophila disk large/zonula occludens-1-containing scaffolding protein synapse-associated protein 97 via its carboxyl terminal domain (amino acids 300-357). Induced ischemia rapidly increased glycosylation of Panx1, resulting in increased trafficking to the plasma membrane as well as increased interaction with synapse-associated protein 97. Cellular stress enhanced ATP release from myocyte Panx1 channels, which, in turn, causes fibroblast transformation to the activated myofibroblast phenotype via activation of the MAPK and p53 pathways, both of which are involved in the development of cardiac fibrosis. ATP release through Panx1 channels in cardiac myocytes during ischemia may be an early paracrine event leading to profibrotic responses to ischemic cardiac injury.
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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.