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Alizadehasl, Azin, Alavi, Maryam Sadat, Alavi, Mohaddeseh Sadat, Roohbakhsh, Ali. (1402). TRPA1 as a promising target in ischemia/reperfusion: A comprehensive review. , 27(3), 270-278. doi: 10.22038/ijbms.2023.74590.16198
Azin Alizadehasl; Maryam Sadat Alavi; Mohaddeseh Sadat Alavi; Ali Roohbakhsh. "TRPA1 as a promising target in ischemia/reperfusion: A comprehensive review". , 27, 3, 1402, 270-278. doi: 10.22038/ijbms.2023.74590.16198
Alizadehasl, Azin, Alavi, Maryam Sadat, Alavi, Mohaddeseh Sadat, Roohbakhsh, Ali. (1402). 'TRPA1 as a promising target in ischemia/reperfusion: A comprehensive review', , 27(3), pp. 270-278. doi: 10.22038/ijbms.2023.74590.16198
Alizadehasl, Azin, Alavi, Maryam Sadat, Alavi, Mohaddeseh Sadat, Roohbakhsh, Ali. TRPA1 as a promising target in ischemia/reperfusion: A comprehensive review. , 1402; 27(3): 270-278. doi: 10.22038/ijbms.2023.74590.16198

TRPA1 as a promising target in ischemia/reperfusion: A comprehensive review

Iranian Journal of Basic Medical Sciences
مقاله 2، دوره 27، شماره 3، خرداد 2024، صفحه 270-278    اصل مقاله (467.84 K)
نوع مقاله: Review Article
شناسه دیجیتال (DOI): 10.22038/ijbms.2023.74590.16198
نویسندگان
Azin Alizadehasl1، 2؛ Maryam Sadat Alavi2؛ Mohaddeseh Sadat Alavi3؛ Ali Roohbakhsh* 4، 5
1Cardio-Oncology Research Center, Rajaie Cardiovascular Medical and Research Center, Iran University of Medical Sciences, Tehran, Iran
2Department of Echocardiography, Rajaie Cardiovascular Medical and Research Center, Iran University of Medical Sciences, Tehran, Iran
3Pharmacological Research Center of Medicinal Plants, Mashhad University of Medical Sciences, Mashhad, Iran
44 Pharmaceutical Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran
5Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
چکیده
Ischemic disorders, including myocardial infarction, cerebral ischemia, and peripheral vascular impairment, are the main common reasons for debilitating diseases and death in Western cultures. Ischemia occurs when blood circulation is reduced in tissues. Reperfusion, although commanded to return oxygen to ischemic tissues, generates paradoxical tissue responses. The responses include generating reactive oxygen species (ROS), stimulating inflammatory responses in ischemic organs, endoplasmic reticulum stress, and the expansion of postischemic capillary no-reflow, which intensifies organ damage. Multiple pathologic processes contribute to ischemia/reperfusion; therefore, targeting different pathologic processes may yield an effective therapeutic approach. Transient Receptor Potential A1 (TRPA1) belongs to the TRP family of ion channels, detects a broad range of chemicals, and promotes the transduction of noxious stimuli, e.g., methylglyoxal, ROS, and acrolein effects are attributed to the channel’s sensitivity to intracellular calcium elevation or phosphoinositol phosphate modulation. Hypoxia and ischemia are associated with oxidative stress, which activates the TRPA1 channel. This review describes the role of TRPA1 and its related mechanisms that contribute to ischemia/reperfusion. Relevant articles were searched from PubMed, Scopus, Web of Sciences, and Google Scholar electronic databases, up to the end of August 2023. Based on the evidence presented here, TRPA1 may have protective or deteriorative functions during the ischemia/reperfusion process. Its function depends on the activation level, the ischemic region, the extent of lesions, and the duration of ischemia.
کلیدواژه‌ها
Inflammation؛ Ischemia؛ Reactive oxygen species؛ Transient receptor potential channels؛ TRPA1 cation channel
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