Research library

Key finding

In mice, MOTS-c activated AMPK-linked metabolic signalling and prevented age-related and high-fat-diet-induced insulin resistance and obesity.

Key finding

MOTS-c increased after exercise in people and restored physical capacity and skeletal-muscle homeostasis in aged mice.

Key finding

In healthy ageing men, skeletal-muscle MOTS-c expression was associated with muscle-fibre composition, linking this mitochondrial peptide to human muscle biology.

Key finding

In mouse and muscle-cell models, MOTS-c reduced myostatin and other atrophy-related signals while supporting muscle metabolism.

Key finding

This review reports that circulating MOTS-c declines with age and synthesizes evidence across glucose metabolism, insulin resistance, inflammation and age-related disease models.

Key finding

Skeletal muscle adapts to aerobic exercise training, in part, through fast-to-slow phenotypic shifts and an expansion of mitochondrial networks.

Key finding

MOTS-c is an exercise mimetic and improves insulin sensitivity in aged and diet-induced obese mice.

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MOTS-c promotes cell differentiation of BMSCs to osteoblasts via TGF-β/Smad pathway.

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Therapeutic targeting bone loss has been the focus of the study in osteoporosis.

Key finding

Cellular homeostasis is coordinated through communication between mitochondria and the nucleus, organelles that each possess their own genomes.

Key finding

Mitochondrial-derived peptides (MDPs) are encoded by the mitochondrial genome and hypothesised to form part of a retrograde signalling network that modulates adaptive responses to metabolic stress.

Key finding

MOTS-c, a mitochondrial-derived peptide (MDP), has been shown to have multiple biological activities such as antioxidation, anti-inflammation, and anti-apoptosis properties.

Key finding

Type 2 Diabetes (T2D) is an emerging public health problem in Asia.

Key finding

The mechanisms that explain mitochondrial dysfunction in aging and healthspan continue to be studied, but one element has been unexplored: microproteins.

Key finding

Low levels of mitochondrial stress are beneficial for organismal health and survival through a process known as mitohormesis.

Key finding

MOTS-c, a 16 amino acid mitochondrial derived peptide, is encoded from the 12S rRNA region of the mitochondrial genome.

Key finding

Acute exercise, and in particular aerobic exercise, increases skeletal muscle energy demand causing mitochondrial stress, and mitochondrial-related adaptations which are a hallmark of exercise training.

Key finding

Mitochondrial-derived peptides (MDPs), encoded by mitochondrial DNA, play a cytoprotective role by helping preserve mitochondrial function and cell viability under stressful conditions.

Key finding

Mitochondria are ancient organelles that are thought to have emerged from once free-living α-proto-bacteria.

Key finding

Mitochondria are key players in aging and in the pathogenesis of age-related diseases.