The proteins of the BCL-2 family are key regulators of mitochondrial apoptosis, acting as
either promoters or inhibitors of cell death. The functional interplay and balance between the …

Mitochondria have cell-type specific phenotypes, perform dozens of interconnected
functions and undergo dynamic and often reversible physiological recalibrations. Given their …

The analogy of mitochondria as powerhouses has expired. Mitochondria are living, dynamic,
maternally inherited, energy-transforming, biosynthetic, and signaling organelles that …

Numerous mitochondrial constituents and metabolic products can function as damage-
associated molecular patterns (DAMPs) and promote inflammation when released into the …

Senescent cells drive age-related tissue dysfunction partially through the induction of a
chronic senescence-associated secretory phenotype (SASP). Mitochondria are major …

Mutations in fumarate hydratase (FH) cause hereditary leiomyomatosis and renal cell
carcinoma. Loss of FH in the kidney elicits several oncogenic signalling cascades through …

The mitochondrial permeability transition (mPT) describes a Ca2+-dependent and
cyclophilin D (CypD)-facilitated increase of inner mitochondrial membrane permeability that …

Gasdermin D (GSDMD)-activated inflammatory cell death (pyroptosis) causes mitochondrial
damage, but its underlying mechanism and functional consequences are largely unknown …

Mitochondrial permeability transition (mPT) is a phenomenon that abruptly causes the flux of
low molecular weight solutes (molecular weight up to 1,500) across the generally …

Mitochondria have recently emerged as key drivers of inflammation associated with cell
death. Many of the pro-inflammatory pathways activated during cell death occur upon …