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Mitochondrial-Derived Peptides in Diabetes and Its Complications
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This review discusses mitochondrial-derived peptides (MDPs) — short peptides formed from open reading frames within human mitochondrial DNA (mtDNA) — and their described roles in diabetes and its complications; species not specified beyond human mtDNA origin. It focuses on MDPs identified so far, including Humanin (HN), mitochondrial open reading frame of the 12S rRNA-c (MOTS-c), and Small humanin-like peptides (SHLP 1-6), discussing their roles in diabetes and its major complications, stroke and myocardial infarction, described as acting via improving insulin resistance, inhibiting inflammatory response, and anti-apoptosis.
Abstract
The changes of mitochondrial function are closely related to diabetes and its complications. Here we describe the effects of mitochondrial-derived peptides (MDPs), short peptides formed by transcription and translation of the open reading frame site in human mitochondrial DNA (mtDNA), on diabetes and its complications. We mainly focus on MDPs that have been discovered so far, such as Humanin (HN), mitochondrial open reading frame of the 12S rRNA-c (MOTS-c) and Small humanin-like peptides (SHLP 1-6), and elucidated the role of MDPs in diabetes and its major complications stroke and myocardial infarction by improving insulin resistance, inhibiting inflammatory response and anti-apoptosis. It provides more possibilities for the clinical application of mitochondrial derived peptides.
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