Currently, obesity is the most common major health problem for people worldwide. Obesity is known to be a significant risk factor for several diseases, including metabolic syndrome, insulin resistance and type 2 diabetes, eventually leading to the development of chronic systemic disorders. Previous studies showed that mitochondrial dysfunction could be one of the potential mechanisms for obesity progression. Most interventions used for combating obesity have also been reported to modulate mitochondrial function, suggesting the potential role of mitochondria in the pathology of the obese condition. Recent studies have shown that peptides produced by mitochondria, mitochondrial-derived peptides (MDPs), potentially improve metabolic function and exert benefits in obesity-associated diabetes and various heart pathologies. In this review, the roles of MDPs in the metabolic pathways and their use in the treatment of various adverse effects of obesity are comprehensively summarised based on collective evidence from in vitro, in vivo and clinical studies. The roles of MDPs as novel therapeutic interventions for cardiac dysfunction caused by various stresses or toxicities are also presented and discussed. This review aims to summarise the knowledge regarding the effects of MDPs on obesity, with a particular emphasis on their potential protective effects on the impaired cardiac function associated with obesity. The information from this review will also encourage further clinical investigations to warrant the potential application of MDP interventions in the clinical setting in the future.
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http://dx.doi.org/10.1136/jcp-2022-208321 | DOI Listing |
Sci Rep
December 2024
Department of Endocrinology, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, China.
High glucose (HG) induced endothelial senescence is related to endothelial dysfunction and cardiovascular complications in diabetic patients. Humanin, a member of mitochondrial derived peptides (MDPs), is thought to contribute to aging-related cardiovascular protection. The goal of the study is to explore the pathogenesis of HG-induced endothelial senescence and potential anti-senescent effects of Humanin.
View Article and Find Full Text PDFFree Radic Biol Med
December 2024
School of Exercise and Health, Shanghai University of Sport, Shanghai, 200438, China. Electronic address:
The mitochondrial open reading frame of 12S rRNA-c (MOTS-c) is a biologically active mitochondria-derived peptide. However, the relationship between MOTS-c, skeletal muscle mitochondrial function, and endurance exercise adaptations is unknown. Here, we tested indices such as maximal oxygen uptake and serum MOTS-c levels in marathon runners and sedentary subjects.
View Article and Find Full Text PDFTrends Genet
December 2024
Leonard Davis School of Gerontology, University of Southern California, Los Angeles, CA, USA.
Given the uniqueness of the mitochondria, and the fact that they have their own genome, mitochondrial-derived microproteins (MDPs) are similar to, but different from, nuclear-encoded microproteins. The discovery of an increasing number of microproteins from this organelle and the importance of mitochondria to cellular and organismal health make it a priority to study this novel class of proteins in search of possible therapeutic targets and cures. In this review, we discuss the history of MDP discovery, describe the function of each MDP, and conclude with future goals and techniques to help discover more MDPs.
View Article and Find Full Text PDFNeuropharmacology
February 2025
Firat University Faculty of Medicine, Department of Biophysics, Elazig, Turkey. Electronic address:
Neuropathic pain is associated with diverse etiologies, including sciatica, diabetes, and the use of chemotherapeutic agents. Despite the varied origins, mitochondrial dysfunction, oxidative stress, and inflammatory cytokines are recognized as key contributing factors in both the initiation and maintenance of neuropathic pain. The effects of the mitochondrial-derived peptide humanin on neuropathic pain, however, remain unclear, despite its demonstrated influence on these mechanisms in numerous disease models.
View Article and Find Full Text PDFFront Immunol
November 2024
Institute of Inflammation and Ageing, University of Birmingham, Birmingham, United Kingdom.
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