François M. Vallette

TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.

TL;DR: The current view on the mitochondrial pathway of apoptosis is presented with a particular attention to new aspects of the regulation of the Bcl-2 proteins family control of mitochondrial membrane permeabilization: the mechanisms implicated in their mitochondrial targeting and activation during apoptosis, the function(s) of the oncosuppressive protein p53 at the mitochondria and the role of the processes of mitochondrial fusion and fission.

TL;DR: Panton-Valentine leukocidin, which belongs to the pore-forming toxin family, could act at the mitochondrion level by creating pores in the mitochondrial outer membrane and was detected in lung sections of patients with necrotizing pneumonia, suggesting that PVL induces apoptosis in vivo and thereby is directly involved in the pathophysiology of necrotized pneumonia.

TL;DR: This review focuses on the molecular events of Bax activation through its interaction with the other proteins from the Bcl-2 family, and the mechanism by which Bax triggers the MOM permeabilization once activated.

TL;DR: It is shown that, in yeast cells grown under nonstarving conditions, autophagy can be induced by mitochondrial dysfunction, and mitochondrial damage-induced Autophagy results in the preferential degradation of impaired mitochondria (mitophagy), before leading to cell death.