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Sepsis triggers mitochondrial impairment in platelets, promoting hyperactivation via ROS production. The mitochondria-specific antioxidant MitoTEMPO reverses these changes in vitro, suggesting therapeutic potential to prevent sepsis-related
Elevated soluble ST2 worsens fulminant myocarditis by impairing cardiomyocyte mitochondria via IGF2R-YY1, providing a new prognostic biomarker and therapeutic target.
This article reviews novel research showing how cytoplasmic mislocalization of RBM20 impairs mitochondrial function, leading to severe dilated cardiomyopathy and highlighting distinct mechanisms between gain- and loss-of-function RBM20 vari
Cheminformatic screening identified novel small molecules with apoptotic, autophagic, and reductase-inhibitory activities that selectively kill AML cells, induce mitochondrial dysfunction, and synergize with current therapies, highlighting
Elamipretide improved skeletal muscle force, titin phosphorylation, and atrophy in a HFpEF rat model, supporting cardiolipin stabilization as a promising mitochondrial-targeted strategy.
In a HFpEF rat model, elamipretide improved skeletal muscle force, reduced titin hyperphosphorylation, and prevented atrophy, supporting cardiolipin stabilization as a promising metabolic strategy.
The APOE ε4 allele significantly reduces survival in Parkinson’s disease patients independently of dementia, linked to mitochondrial dysfunction and ER stress in PD models.
Long COVID patients exhibit distinct mitochondrial bioenergetic impairments, with altered ATP synthase function correlating with clinical symptoms and quality of life, implicating mitochondrial dysfunction in its pathogenesis.
