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Int J Mol Sci. 2018 Jan 31;19(2). pii: E417. doi: 10.3390/ijms19020417.

Interplay between ROS and Antioxidants during Ischemia-Reperfusion Injuries in Cardiac and Skeletal Muscle.

Author information

1
Radiologic Sciences and Respiratory Therapy Division, School of Health and Rehabilitation Sciences, The Ohio State University College of Medicine, The Ohio State University Wexner Medical Center, Columbus, OH 43210, USA. zhou.1273@osu.edu.
2
Interdisciplinary Biophysics Graduate Program, The Ohio State University, Columbus, OH 43210, USA. zhou.1273@osu.edu.
3
Radiologic Sciences and Respiratory Therapy Division, School of Health and Rehabilitation Sciences, The Ohio State University College of Medicine, The Ohio State University Wexner Medical Center, Columbus, OH 43210, USA. prather.50@buckeyemail.osu.edu.
4
Radiologic Sciences and Respiratory Therapy Division, School of Health and Rehabilitation Sciences, The Ohio State University College of Medicine, The Ohio State University Wexner Medical Center, Columbus, OH 43210, USA. garrison.189@buckeyemail.osu.edu.
5
Radiologic Sciences and Respiratory Therapy Division, School of Health and Rehabilitation Sciences, The Ohio State University College of Medicine, The Ohio State University Wexner Medical Center, Columbus, OH 43210, USA. zuo.4@osu.edu.
6
Interdisciplinary Biophysics Graduate Program, The Ohio State University, Columbus, OH 43210, USA. zuo.4@osu.edu.

Abstract

Ischemia reperfusion (IR), present in myocardial infarction or extremity injuries, is a major clinical issue and leads to substantial tissue damage. Molecular mechanisms underlying IR injury in striated muscles involve the production of reactive oxygen species (ROS). Excessive ROS accumulation results in cellular oxidative stress, mitochondrial dysfunction, and initiation of cell death by activation of the mitochondrial permeability transition pore. Elevated ROS levels can also decrease myofibrillar Ca2+ sensitivity, thereby compromising muscle contractile function. Low levels of ROS can act as signaling molecules involved in the protective pathways of ischemic preconditioning (IPC). By scavenging ROS, antioxidant therapies aim to prevent IR injuries with positive treatment outcomes. Novel therapies such as postconditioning and pharmacological interventions that target IPC pathways hold great potential in attenuating IR injuries. Factors such as aging and diabetes could have a significant impact on the severity of IR injuries. The current paper aims to provide a comprehensive review on the multifaceted roles of ROS in IR injuries, with a focus on cardiac and skeletal muscle, as well as recent advancement in ROS-related therapies.

KEYWORDS:

contraction; cytochrome c; free radicals; ischemic preconditioning

PMID:
29385043
PMCID:
PMC5855639
DOI:
10.3390/ijms19020417
[Indexed for MEDLINE]
Free PMC Article

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