Enhancing Cardiomyocyte Resilience to Ischemia-Reperfusion Injury: The Therapeutic Potential of an Indole-Peptide-Tempo Conjugate (IPTC)

Ischemia/reperfusion (I/R) injury leads to apoptosis and extensive cellular and mitochondrial damage, triggered by the early generation and subsequent accumulation of mitochondrial reactive oxygen species (mtROS). This condition not only contributes to the pathology of I/R injury itself but is also implicated in a variety of other diseases, especially within the cardiovascular domain. Addressing mitochondrial oxidative stress thus emerges as a critical therapeutic target. In this context, our study introduces an indole-peptide-tempo conjugate (IPTC), a compound designed with dual functionalities: antioxidative properties and the ability to modulate autophagy. Our findings reveal that IPTC effectively shields H9C2 cardiomyocytes against hypoxia/reoxygenation (H/R) damage, primarily through counteracting mtROS overproduction linked to impaired mitophagy and mitochondrial dysfunction. We propose that IPTC operates by simultaneously reducing mtROS levels and inducing mitophagy, highlighting its potential as a novel therapeutic strategy for mitigating mitochondrial oxidative damage and, by extension, easing I/R injury and potentially other related cardiovascular conditions.

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Publication Details

Journal
ACS Omega
Published
2024-09-13
DOI
https://doi.org/10.1021/acsomega.4c02725
Citations
3
Primary Topic
Cardiac Ischemia and Reperfusion
Type
article
Field-Weighted Citation Impact
1.27

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article

Enhancing Cardiomyocyte Resilience to Ischemia-Reperfusion Injury: The Therapeutic Potential of an Indole-Peptide-Tempo Conjugate (IPTC)

K. Michael Gibson, Steffen Jockusch, Xin Yan, Shanshan Hou et al.
3 citations
ACS Omega
Cardiac Ischemia and Reperfusion
1.27
article

Enhancing Cardiomyocyte Resilience to Ischemia-Reperfusion Injury: The Therapeutic Potential of an Indole-Peptide-Tempo Conjugate (IPTC)

K. Michael Gibson, Steffen Jockusch, Xin Yan, Shanshan Hou, Lanrong Bi, Zhiying Shan, Xiang Gao
article en
3 citations

Abstract

Ischemia/reperfusion (I/R) injury leads to apoptosis and extensive cellular and mitochondrial damage, triggered by the early generation and subsequent accumulation of mitochondrial reactive oxygen species (mtROS). This condition not only contributes to the pathology of I/R injury itself but is also implicated in a variety of other diseases, especially within the cardiovascular domain. Addressing mitochondrial oxidative stress thus emerges as a critical therapeutic target. In this context, our study introduces an indole-peptide-tempo conjugate (IPTC), a compound designed with dual functionalities: antioxidative properties and the ability to modulate autophagy. Our findings reveal that IPTC effectively shields H9C2 cardiomyocytes against hypoxia/reoxygenation (H/R) damage, primarily through counteracting mtROS overproduction linked to impaired mitophagy and mitochondrial dysfunction. We propose that IPTC operates by simultaneously reducing mtROS levels and inducing mitophagy, highlighting its potential as a novel therapeutic strategy for mitigating mitochondrial oxidative damage and, by extension, easing I/R injury and potentially other related cardiovascular conditions.

ACS OmegaVol. 9(38)
Michigan Technological University (US), Bowling Green State University (US), Washington State University Spokane (US)
American Heart Association, National Heart, Lung, and Blood Institute
Openalex Percentile: Top 20%
Cardiac Ischemia and Reperfusion
1.27
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