https://journals.umt.edu.pk/index.php/ihr/issue/feed 2026-01-13T05:57:54+00:00 Open Journal Systems <p style="text-align: justify;">International Health Review (IHR) is an open access peer-reviewed biannual journal that strives to lead the debate on multidisciplinary aspects of health and medical sciences and to publish high value productive research through a rigorous process of peer-review and evaluation in the field of health and medical sciences. The journal’s mission is to bring novel, significant, enduring, and advance research of prime importance to health practitioners, researchers and medical experts that addresses challenging questions in health and medical disciplines.</p> https://journals.umt.edu.pk/index.php/ihr/article/view/4919 2026-01-13T05:57:54+00:00 Farwa Munir [email protected] Farooq Manzoor [email protected] Shahzaib Naeem [email protected] Emad Abdulrahman H. Alsaedi [email protected] Maryum Hamayoun [email protected] Sher Wali Khan [email protected] Atif Amin Baig [email protected]

<p>Skeletal muscle mass is strongly linked to stressors like ischemia and reactive oxygen species (ROS), both of which are regulated by oxygen availability and redox homeostasis. Intermittent ischemia and reperfusion cause a burst of reactive oxygen species, destruction of mitochondrial integrity, and inflammatory/necrotic pathways The objective of this review is to summarise existing data on the mechanistic interaction between hypoxia, ROS generation, and necrosis in skeletal muscle, as well as the role of these mechanisms in contributing to ischemia-reperfusion injury, metabolic disruption and dysfunction of skeletal muscle in the long term. The keywords examined in the literature search were skeletal muscle, hypoxia, reactive oxygen species, ischemia-reperfusion, mitochondria, and necrosis using PubMed, Scopus, and Web of Science. Articles published in English between 1990 and 2023 were peer reviewed and included, while conference abstracts, non-scientific reports, and duplicate records were excluded. The evidence suggests that hypoxia changes the use of substrates in the mitochondrion, stabilises the hypoxia-inducible factors and preconditions the muscle fibres to oxidative damage. The overproduction of ROS during reperfusion further increases the activity of inflammatory signalling, like NF-kB, calcium overload, and apoptotic and necrotic cell death. These teamed disruptions are what cause structural disintegration, dysfunctional contractional performance and retarded recuperation. An improved insight into these interrelated processes identifies prospects in therapeutic approaches such as antioxidants, enzymatic inhibition, gene-based treatment, cytokine therapy, and cell-derived exosomes- to alleviate ROS-related damage and promote muscle recovery.</p>

2025-11-15T00:00:00+00:00 Copyright (c) 2025 Farwa Munir, Farooq Manzoor, Shahzaib Naeem, Emad Abdulrahman H. Alsaedi, Maryum Hamayoun, Sher Wali Khan, Atif Amin Baig