In mice, opioids and methamphetamine (but not natural rewards) trigger calcium influx through the mitochondrial calcium uniporter in dopamine-releasing nerve terminals, fueling the rapid ATP production that sustains drug-driven dopamine surges. Blocking this mitochondrial calcium channel genetically or pharmacologically reduced drug-induced dopamine release and addictive behavior without disrupting normal reward processing, pointing to it as a possible addiction drug target.
Read source →A new nanobody-based delivery system precisely targets healthy donor mitochondria to damaged neurons, cardiac cells, and other specific cell types — rescuing degenerating neurons in both a human optic-nerve-atrophy cell model and mice. Still preclinical, but a concrete step toward treating primary mitochondrial diseases like TK2 deficiency.
Read source →In a placebo-controlled RCT of 50 healthy middle-aged adults, 1,000 mg/day of urolithin A for 4 weeks expanded naive, less-exhausted CD8+ T cells and measurably increased mitochondrial biogenesis within those immune cells — a rare case of a supplement showing a measurable immune-aging effect this quickly. Conducted with the Buck Institute for Research on Aging.
Read source →A 4-month, placebo-controlled RCT (NCT03464500) found ~12% gains in muscle strength and improved mitochondrial biomarkers (lower plasma acylcarnitines and CRP) from the mitophagy-activating postbiotic Urolithin A.
Read source →In transgenic mouse models, the mitochondrial-derived peptide MOTS-c boosted intrinsic muscle mitochondrial bioenergetics and lowered ROS-related oxidative damage — requiring both PGC-1α and AMPK signalling, without increasing raw mitochondrial volume. Animal data only; a human Phase 2a trial (MOTS-MET) for prediabetes began enrolling in 2026.
Read source →Using bioinformatic and protein-docking analysis, researchers compared the mitochondrial-derived peptide humanin across mammals with different oxidative-stress profiles (deep-diving cetaceans, high-metabolism shrews, long-lived primates). Species under greater oxidative stress carried more structurally stable humanin variants, suggesting evolution has tuned the peptide's protective function and offering a template for designing humanin-based therapeutic analogs.
Read source →Preclinical work showing MOTS-c, an mtDNA-encoded peptide, restores mitochondrial respiration and energy homeostasis in a type 2 diabetic cardiac model — building the mechanistic case for its "exercise mimetic" reputation.
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