Preprint Article Version 1 Preserved in Portico This version is not peer-reviewed

A Novel Mitophagy Enhancer Protects Cardiomyocytes against Hypoxia/Reoxygenation

Version 1 : Received: 17 August 2022 / Approved: 18 August 2022 / Online: 18 August 2022 (14:33:17 CEST)

How to cite: Yan, X.; Gao, X.; Hou, S.; Jockusch, S.; Gibson, K.M.; Bi, L. A Novel Mitophagy Enhancer Protects Cardiomyocytes against Hypoxia/Reoxygenation. Preprints 2022, 2022080352 (doi: 10.20944/preprints202208.0352.v1). Yan, X.; Gao, X.; Hou, S.; Jockusch, S.; Gibson, K.M.; Bi, L. A Novel Mitophagy Enhancer Protects Cardiomyocytes against Hypoxia/Reoxygenation. Preprints 2022, 2022080352 (doi: 10.20944/preprints202208.0352.v1).

Abstract

Ischemia/reperfusion (I/R) injury results in cell death by inducing apoptosis. During I/R, early generation of mitochondrial reactive oxygen species (mtROS) can induce neighboring mitochondria to release additional ROS, a toxic cycle resulting in significant mitochondrial and cellular injury. Oxidative damage in the mitochondria contributes to various pathologies, including I/R injury. Accordingly, preventing mitochondrial oxidative damage should be therapeutically relevant for many disorders, including cardiovascular diseases. We recently discovered an Indole-Peptide-Tempo Conjugate (IPTC) that served as a novel bifunctional agent with both antioxidant and autophagy-modulating capacity. Here, we demonstrate that IPTC can protect H9C2 cardiomyocytes from hypoxia/reoxygenation (H/R) injury that results from mtROS overproduction due to impaired mitophagy and resultant mitochondrial dysfunction. We hypothesize that the mechanism of action of IPTC involves the capacity to decrease mtROS combined with induction of mitophagy.

Keywords

Oxidative Stress, Free radical scavenging, Autophagy, Ischemia/reperfusion injury, Hypox-ia/reoxygenation, Mitophagy

Subject

CHEMISTRY, Medicinal Chemistry

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