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Proposed mechanism for the role of DIAPH1 in I/R injury. DIAPH1 is upregulated following I/R injury, which leads to an increase in actin polymerization. This allows for stimulation of SRF and myocardin, which results in elevated SRF-regulated gene transcription as well as increased EGR1. SRF also stimulates NCX1 expression. Downstream of EGR1, SERCA2a is reduced. The changes in NCX1 and SERCA2a expression contribute to injury and dysfunction in the myocardium.
