ArticleJCI insight2018
Stress response protein GJA1-20k promotes mitochondrial biogenesis, metabolic quiescence, and cardioprotection against ischemia/reperfusion injury.
Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
59 citing papers in PubMed, 1 synthesis or guideline pooled it, 87 citations in OpenAlex.
- Using human induced pluripotent stem cell-derived cardiomyocytes to understand the mechanisms driving cardiomyocyte maturation.Frontiers in cardiovascular medicine · 2022Pooled it
- From channels to communication networks: a perspective on connexins, pannexins and innexins.Cell and tissue research · 2026Article
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- Mitochondrial DNA mutations drive tumor heterogeneity in papillary thyroid carcinoma.iScience · 2026Article
- Loss of connexin 43 in cartilage causes mitochondrial dysfunction and accelerates post-traumatic osteoarthritis progression.bioRxiv : the preprint server for biology · 2026Article
- Cardioprotective effects of prolyl hydroxylase inhibitors during reperfusion in myocardial infarction: A study using cardiosphere-derived cells.Experimental physiology · 2026Article
- Connexin 26 Functions as a Direct Transcriptional Regulator During the Cochlea Development.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- FASN-mediated metabolic reprogramming drives CD4Arthritis research & therapy · 2026Article
- Inhibition of Pyk2 prevents Cx43 remodeling and cardiomyocyte injury during hypoxic and adrenergic stress.Journal of molecular and cellular cardiology · 2026Article
- Injectable platelet-rich plasma-based hydrogels: a controlled release platform for growth factors and cardiac regeneration post-myocardial infarction.Regenerative biomaterials · 2026Article
- The role of mitochondrial transfer in lung disease.Respiratory research · 2025Review
- Comparative transcriptome analysis of pectoralis major muscles affected by white striping, wooden breast and spaghetti meat in male and female broiler chickens.BMC genomics · 2025Article
- Mitochondrial Quality Control in Health and Disease.MedComm · 2025Review
- Left Ventricular Unloading With Assist Device Implantation Increases GJA1-20k Expression in Patients With Arrhythmogenic Cardiomyopathy.Circulation. Heart failure · 2025Article
- Article
- Overexpression of Cx43: Is It an Effective Approach for the Treatment of Cardiovascular Diseases?Biomolecules · 2025Review
- A truncated isoform of Connexin43 caps actin to organize forward delivery of full-length Connexin43.The Journal of cell biology · 2025Article
- Review
- Review
- Connexin 43 regulates intercellular mitochondrial transfer from human mesenchymal stromal cells to chondrocytes.Stem cell research & therapy · 2024Article
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 1 institution in 1 country.
Funding
Abstract
Connexin 43 (Cx43), a product of the GJA1 gene, is a gap junction protein facilitating intercellular communication between cardiomyocytes. Cx43 protects the heart from ischemic injury by mechanisms that are not well understood. GJA1 mRNA can undergo alternative translation, generating smaller isoforms in the heart, with GJA1-20k being the most abundant. Here, we report that ischemic and ischemia/reperfusion (I/R) injuries upregulate endogenous GJA1-20k protein in the heart, which targets to cardiac mitochondria and associates with the outer mitochondrial membrane. Exploring the functional consequence of increased GJA1-20k, we found that AAV9-mediated gene transfer of GJA1-20k in mouse hearts increases mitochondrial biogenesis while reducing mitochondrial membrane potential, respiration, and ROS production. By doing so, GJA1-20k promotes a protective mitochondrial phenotype, as seen with ischemic preconditioning (IPC), which also increases endogenous GJA1-20k in heart lysates and mitochondrial fractions. As a result, AAV9-GJA1-20k pretreatment reduces myocardial infarct size in mouse hearts subjected to in vivo ischemic injury or ex vivo I/R injury, similar to an IPC-induced cardioprotective effect. In conclusion, GJA1-20k is an endogenous stress response protein that induces mitochondrial biogenesis and metabolic hibernation, preconditioning the heart against I/R insults. Introduction of exogenous GJA1-20k is a putative therapeutic strategy for patients undergoing anticipated ischemic 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.