Škrlec I, Kolomeichuk SN. Hypoxia-inducible factor-1α in myocardial infarction. World J Cardiol 2024; 16(4): 181-185 [PMID: 38690212 DOI: 10.4330/wjc.v16.i4.181]
Corresponding Author of This Article
Ivana Škrlec, MSc, PhD, Assistant Professor, Faculty of Dental Medicine and Health, Josip Juraj Strossmayer University of Osijek, Crkvena 21, Osijek 31000, Croatia. iskrlec@fdmz.hr
Research Domain of This Article
Biochemistry & Molecular Biology
Article-Type of This Article
Editorial
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Cardiol. Apr 26, 2024; 16(4): 181-185 Published online Apr 26, 2024. doi: 10.4330/wjc.v16.i4.181
Hypoxia-inducible factor-1α in myocardial infarction
Ivana Škrlec, Sergey N Kolomeichuk
Ivana Škrlec, Faculty of Dental Medicine and Health, Josip Juraj Strossmayer University of Osijek, Osijek 31000, Croatia
Sergey N Kolomeichuk, Institute of Biology, Karelia Research Center of Russian Academy of Sciences, Petrozavodsk 185910, Russia
Sergey N Kolomeichuk, Laboratory for Genomics, Proteomics, and Metabolomics, Research Institute of Biomedicine and Biomedical Technologies, Tyumen State Medical University, Tyumen 625023, Russia
Author contributions: Škrlec I did the majority of the writing and prepared the figure; Kolomeychuk SN did some writing and text editing.
Supported byCroatian Ministry of Science and Education, Josip Juraj Strossmayer University of Osijek, Faculty of Dental Medicine and Health, Osijek, Croatia, No. IP7-FDMZ-2023; West-Siberian Science and Education Center, Government of Tyumen District, Decree of 20.11.2020, No. 928-rp; and Ministry of Science and Higher Education, No. FMEN 2022-0009.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Ivana Škrlec, MSc, PhD, Assistant Professor, Faculty of Dental Medicine and Health, Josip Juraj Strossmayer University of Osijek, Crkvena 21, Osijek 31000, Croatia. iskrlec@fdmz.hr
Received: December 13, 2023 Peer-review started: December 13, 2023 First decision: January 15, 2024 Revised: January 26, 2024 Accepted: March 4, 2024 Article in press: March 4, 2024 Published online: April 26, 2024 Processing time: 131 Days and 23.5 Hours
Abstract
Hypoxia-inducible factor 1 (HIF1) has a crucial function in the regulation of oxygen levels in mammalian cells, especially under hypoxic conditions. Its importance in cardiovascular diseases, particularly in cardiac ischemia, is because of its ability to alleviate cardiac dysfunction. The oxygen-responsive subunit, HIF1α, plays a crucial role in this process, as it has been shown to have cardioprotective effects in myocardial infarction through regulating the expression of genes affecting cellular survival, angiogenesis, and metabolism. Furthermore, HIF1α expression induced reperfusion in the ischemic skeletal muscle, and hypoxic skin wounds in diabetic animal models showed reduced HIF1α expression. Increased expression of HIF1α has been shown to reduce apoptosis and oxidative stress in cardiomyocytes during acute myocardial infarction. Genetic variations in HIF1α have also been found to correlate with altered responses to ischemic cardiovascular disease. In addition, a link has been established between the circadian rhythm and hypoxic molecular signaling pathways, with HIF1α functioning as an oxygen sensor and circadian genes such as period circadian regulator 2 responding to changes in light. This editorial analyzes the relationship between HIF1α and the circadian rhythm and highlights its significance in myocardial adaptation to hypoxia. Understanding the changes in molecular signaling pathways associated with diseases, specifically cardiovascular diseases, provides the opportunity for innovative therapeutic interventions, especially in low-oxygen environments such as myocardial infarction.
Core Tip: Hypoxia-inducible factor 1 (HIF1), a versatile transcription factor, is crucial for the maintenance of oxygen homeostasis. Genetic variations in HIF1α may influence tissue response to hypoxia and affect clinical manifestations of coronary atherosclerosis. Research has confirmed that sufficient HIF1α expression leads to reperfusion in the ischemic skeletal muscle, whereas decreased expression is associated with hypoxic skin wounds in diabetic animal models. In addition, the HIF1α response can be influenced by circadian proteins. Interpretation of circadian and hypoxia signaling pathways may enable therapeutic interventions in diseases associated with oxygen deprivation, including myocardial infarction.
