An oral drug has shown promise for treating metabolic syndrome in mouse models by selectively blocking the production of free radicals in the mitochondria, a research group has found. The study, carried out by a group led by Martin Brand, Professor Emeritus at the Buck Institute for Research on Aging, could lead to treatments that tackle the underlying causes of metabolic syndrome and multiple other conditions linked to aging.

Evidence of mitochondrial and lysosome dysfunction underlying Parkinson’s disease (PD) was discussed during several talks at the World Parkinson Congress 2023 (WPC) held in Barcelona. Edward A. Fon, from McGill University in Montreal, explained how eyes turned to mitochondria as key players in PD more than 30 years ago and how the explosion of genetics was fundamental to advance the knowledge and research in PD.

Over the past decade there has been much research into the use of induced pluripotent stem cells (iPSCs) as a cell therapy to regenerate tissue and treat heart disease. Now, one researcher has narrowed the focus down to treating heart disease not with whole cells, but with mitochondria derived from iPSCs. Gentaro Ikeda, a researcher at the Department of Medicine at Stanford University, has worked on generating extracellular vesicles (EVs) containing mitochondria from pluripotent stem cell-derived cardiomyocytes and administering these to restore the functionality of the myocardium in a porcine model of an infarct.

By interfering with mitochondrial plasticity, researchers have succeeded in attenuating brain metastases of HER2-expressing breast tumors. The authors wrote that their findings “highlight targeting mitochondrial dynamics is a viable therapeutic opportunity to limit both brain tumors and metastasis.”

Researchers from The Salk Institute have described a signaling pathway that sets off an unusual, autophagy-dependent cell death mechanism as a fail-safe for cells that have evaded senescence mechanisms. The scientists found a tumor suppression mechanism mediated by telomere signaling, which activated an innate immune response through mitochondrial and telomere complexes to eliminate cells with shortened telomeres.

Researchers from the University of Zaragoza and Promontory Therapeutics Inc. have discovered that PT-112, which has a multimodal mechanism of action, could have different clinical applications in cancer treatment due to its effects on mitochondria in castration-resistant prostate cancer (CRPC). PT-112 is an immunogenic small molecule currently in phase II development in metastatic castration-resistant prostate cancer (mCRPC). The researchers designed PT-112 to target advanced solid tumors, such as thymus, small-cell, non-small-cell lung or CRPC.