Evolutionary loss of foot muscle in a bipedal rodent shares similarities with skeletal muscle atrophy, which is typically considered a pathological response to injury or disease.

Manipulating cell death in situ with the temporal and spatial precision of optogenetic tools opens up new avenues for studying inflammation, death and related phenomena, revealing, for example, that epithelial cell death cannot be classified into strictly distinct categories.

Genetic analyses using a new oral infection mouse model demonstrate that cell death pathways protect against the gastrointestinal bacterial pathogen Shigella flexneri.

ADeS, a novel deep learning approach for apoptosis detection, achieves 98% accuracy in vitro and in vivo while providing unprecedented insights into the spatial–temporal foundation of cell death.

A pathway controlling non-apoptotic developmental cell death engages non-canonical death-promoting activities of the stress factor HSF-1, which, in turn, activates specific components of the ubiquitin-mediated degradation machinery.

Molecular pathways controlling autophagic cell death are regulated at the level of the lysosome through the activity of the pro-death Bcl-2 family member Bax/Bak.

Src, an oncogene, promotes both cell proliferation and cell death simultaneously, which can be regulated by dietary methionine.

Mitochondrial quality control in the germline is mediated by regulators of both programmed cell death and the aging program.

The proteins Bax and Bak, which increase the permeability of the mitochondrial membrane during apoptosis, are also crucial for generating a mitochondrial membrane pore that is specifically involved in necrosis.

A novel pathway was discovered for cellular uptake of LPS through secretory protein secretoglobin3A2 and a receptor syndecan-1, causing activation of non-canonical inflammasome pathway leading to pyroptosis of cancer cells.