Jin Wang

TL;DR: It is demonstrated that casein kinase 2α (CK2α) was upregulated following acute cardiac IR injury and confirmed that CK2α serves as a negative regulator of mitochondrial homeostasis via suppression of FUNDC1-required mitophagy, favoring the development of cardiac IR injuries.

TL;DR: It is illustrated that NR4A1 serves as a novel culprit factor in cardiac microvascular IR injury that operates through synchronous elevation of fission and suppression of mitophagy and novel therapeutic strategies targeting the balance might provide survival advantage to microvasculature following IR stress.

TL;DR: The involvement of mROS and mitochondrial morphofunction in cardiac microvascular I/R injury is discussed.

TL;DR: The results demonstrated that Ripk3 was primarily activated by IR injury and consequently aggravated endothelial necroptosis, microvessel barrier dysfunction, capillary hyperpermeability, the inflammation response, microcirculatory vasospasms, and microvascular perfusion defects, and administration of melatonin prevented RipK3 activation and provided a pro‐survival advantage for the endothelial system in the context of cardiac IR injury.

TL;DR: Fundc1 mitophagy, primarily driven by IPC, confers resistance to AKI through reconciliation of mitochondrial fission, implicating the therapeutic potential of targeting mitochondrial homeostasis for AKI.