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Cardio-protective role of Humanin in myocardial ischemia-reperfusion

Review · human · Biochimica et biophysica acta. General subjects · 2022 · DOI 10.1016/j.bbagen.2021.130066 · PMID 34896254

Plain-language summary

Paraphrased from the published abstract below — not a verdict on whether anything works.

This minireview discusses humanin, a 24-amino-acid mitochondria-derived peptide (MDP) first identified in 2001 in surviving neurons of a patient with Alzheimer's disease, summarizing reported roles for humanin and related MDPs (including MOTS-c and SHLP1-6) in aging, metabolic disorders, cardiovascular disease, and autoimmune disease, and its associations with autophagy, ER stress, cellular metabolism, oxidative stress, and inflammation. It reviews literature describing humanin's proposed role in cardio-protection following myocardial ischemia-reperfusion injury, including in coronary heart disease, atherosclerosis, and myocardial fibrosis, and discusses potential underlying mechanisms, without presenting new experimental data of its own.

Abstract

Mitochondria-derived peptides (MDPs) are bioactive peptides encoded by and secreted from the mitochondria. To date, a few MDPs including humanin, MOTS-c and SHLP1-6, and their diverse biological functions have been identified. The first and most studied MDP is humanin, a 24-amino-acid poly peptide. It was first identified in 2001 in the surviving neurons of patient with Alzheimer's disease, and since then has been well characterized for its neuro-protective effect through inhibition of apoptosis. Over the past two decades, humanin has been reported to play critical roles in aging as well as multiple diseases including metabolic disorders, cardiovascular diseases, and autoimmune disease. Humanin has been shown to modulate multiple biological processes including autophagy, ER stress, cellular metabolism, oxidative stress, and inflammation. A role for humanin has been shown in a wide range of cardiovascular diseases, such as coronary heart disease, atherosclerosis, and myocardial fibrosis. In this minireview, we will summarize the literature demonstrating a role for humanin in cardio-protection following myocardial ischemia-reperfusion induced injury and the potential mechanisms that mediate it.

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