Corrigendum to “Connexin 43 dephosphorylation at serine 282 induces spontaneous arrhythmia and increases susceptibility to ischemia/reperfusion injury” [Heliyon 9 (5), May 2023 Article e15879]

In the original published version of this article, there is a mistake in Fig. 2A. The authors have attached the revised version of Figure 2 and wish to replace it in the article. The correct version of figure can be found below. The authors apologize for the errors. Both the HTML and PDF versions of the article have been updated to correct the errors. Connexin 43 dephosphorylation at serine 282 induces spontaneous arrhythmia and increases susceptibility to ischemia/reperfusion injuryWu et al.HeliyonApril 30, 2023In BriefConnexin 43 (Cx43), the predominant gap junction protein in hearts, is modified by specific (de)phosphorylation events under physiological and pathological states to affect myocardium function and structure. Previously we found that deficiency in Cx43 S282 phosphorylation could impair intercellular communication and contribute to cardiomyocyte apoptosis by activating p38 mitogen-activated protein kinase (p38 MAPK)/factor-associated suicide (Fas)/Fas-associating protein with a novel death domain (FADD) pathway, which is involved in myocardium injury in ischemia/reperfusion (I/R) heart. Full-Text PDF Open Access