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In this study, researchers found that mitochondrial complex I plays a crucial role in regulating innate immunity and bone remodeling, with Ndufs4 deletion causing systemic inflammation and osteopetrosis through various metabolic shifts and cellular mechanisms.

Martin-Perez et al. show that rapamycin's beneficial effects in a mouse model of Leigh syndrome are linked to the downregulation of protein kinase C.

This study found that in a mouse model of Leigh syndrome, rapamycin alters brain proteome and may extend survival by targeting protein kinase C.

This study suggests that inhibiting PKC, similar to rapamycin treatment, can extend lifespan and reduce neurological symptoms and inflammation in mice with mitochondrial dysfunction, potentially involving the mTORC2 pathway.