ArticleCardiovascular research2023
Mitochondrial pannexin1 controls cardiac sensitivity to ischaemia/reperfusion injury.
Article in Cardiovascular research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- Pannexins in the heart: cell-specific expression and contributions to disease.Cell and tissue research · 2026Review
- METTL1-Mediated NMedComm · 2026Article
- Modified mRNA-Based Therapeutic Strategies for Myocardial Ischemia-Reperfusion Injury.International journal of molecular sciences · 2025Review
- Pannexins in the vasculature.American journal of physiology. Heart and circulatory physiology · 2025Review
- Pannexin channels in the kidney.American journal of physiology. Renal physiology · 2025Review
- Nanobody-based Pannexin1 channel inhibitors increase survival after cardiac ischemia/reperfusion.Cell and tissue research · 2025Article
- Proximal tubule pannexin 1 contributes to mitochondrial dysfunction and cell death during acute kidney injury.American journal of physiology. Renal physiology · 2025Article
- Adenosine triphosphate-induced cell death in heart failure: Is there a link?World journal of cardiology · 2025Review
- Pannexin channels in inflammation and tumorigenesis.Frontiers in cell and developmental biology · 2025Review
- Cold Exposure Rejuvenates the Metabolic Phenotype ofBiomolecules · 2024Article
- Cardiomyocyte PANX1 Controls Glycolysis and Neutrophil Recruitment in Hypertrophy.Circulation research · 2024Article
- Aging-induced mitochondrial dysfunction: two distinct populations of mitochondria versus a combined population.American journal of physiology. Heart and circulatory physiology · 2024Article
- Hemichannels contribute to mitochondrial CaFrontiers in cell and developmental biology · 2024Article
- Intercellular Communication in Airway Epithelial Cell Regeneration: Potential Roles of Connexins and Pannexins.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsNo effective therapy is available in clinics to protect the heart from ischaemia/reperfusion (I/R) injury. Endothelial cells are activated after I/R, which may drive the inflammatory response by releasing ATP through pannexin1 (Panx1) channels. Here, we investigated the role of Panx1 in cardiac I/R. METHODS AND
resultsPanx1 was found in cardiac endothelial cells, neutrophils, and cardiomyocytes. After in vivo I/R, serum Troponin-I, and infarct size were less pronounced in Panx1-/- mice, but leukocyte infiltration in the infarct area was similar between Panx1-/- and wild-type mice. Serum Troponin-I and infarct size were not different between mice with neutrophil-specific deletion of Panx1 and Panx1fl/fl mice, suggesting that cardioprotection by Panx1 deletion rather involved cardiomyocytes than the inflammatory response. Physiological cardiac function in wild-type and Panx1-/- hearts was similar. The time to onset of contracture and time to maximal contracture were delayed in Panx1-/- hearts, suggesting reduced sensitivity of these hearts to ischaemic injury. Moreover, Panx1-/- hearts showed better recovery of left ventricle developed pressure, cardiac contractility, and relaxation after I/R. Ischaemic preconditioning failed to confer further protection in Panx1-/- hearts. Panx1 was found in subsarcolemmal mitochondria (SSM). SSM in WT or Panx1-/- hearts showed no differences in morphology. The function of the mitochondrial permeability transition pore and production of reactive oxygen species in SSM was not affected, but mitochondrial respiration was reduced in Panx1-/- SSM. Finally, Panx1-/- cardiomyocytes had a decreased mitochondrial membrane potential and an increased mitochondrial ATP content.
conclusionPanx1-/- mice display decreased sensitivity to cardiac I/R injury, resulting in smaller infarcts and improved recovery of left ventricular function. This cardioprotective effect of Panx1 deletion seems to involve cardiac mitochondria rather than a reduced inflammatory response. Thus, Panx1 may represent a new target for controlling cardiac reperfusion damage.
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