Moshi Song

TL;DR: Parallel studies in cultured murine embryonic fibroblasts and in vivo mouse hearts revealed that Mfn1/Mfn2 deletion provoked accumulation of defective mitochondria exhibiting an unfolded protein response, without appropriately increasing mitophagy, and interrupting mitochondrial fission by Drp1 ablation increased mitophileagy and caused a generalized loss of mitochondria.

TL;DR: It is posited that mitochondria optimized for a given metabolic milieu must be replaced when conditions change, as during the perinatal period, and late fetal and adult cardiomyocyte mitochondria have distinct morphologies as well as metabolic preferences.

TL;DR: A comprehensive understanding of the cell-type-specific mechanisms underlying primate ovarian aging at single-cell resolution is provided, revealing new diagnostic biomarkers and potential therapeutic targets for age-related human ovarian disorders.

TL;DR: Accumulating evidence supporting important roles for mitochondrial fission and fusion in cardiac mitochondrial quality control is reviewed, focusing on the PTEN-induced putative kinase 1-Parkin mitophagy pathway.

TL;DR: Cardiomyopathies linked to dynamic imbalance between fission and fusion are temporarily mitigated by forced mitochondrial adynamism at the cost of compromising mitochondrial quantity control and accelerating mitochondrial senescence.