Michael T. Lotze

TL;DR: These features of HMGB1 are discussed and recent advances that have led to the preclinical development of therapeutics that modulateHMGB1 release and activity are summarized.

TL;DR: It is demonstrated that autophagy contributes to ferroptosis by degradation of ferritin in fibroblasts and cancer cells by knocking out or knockdown of Atg5 and Atg7, which provides novel insight into the interplay between Autophagy and regulated cell death.

TL;DR: High-mobility group box 1 (HMGB1), the most abundant and well-studied HMG protein, senses and coordinates the cellular stress response and plays a critical role not only inside of the cell as a DNA chaperone, chromosome guardian, autophagy sustainer, and protector from apoptotic cell death, but also outside thecell as the prototypic damage associated molecular pattern molecule (DAMP).

TL;DR: It is provocatively suggested that adult cancer results from rounds of disordered and unscheduled necrotic cell death, subsequent epithelial proliferation and the resulting suppressed immunity, rather than from a process that is dictated solely by cell growth.

TL;DR: It is speculated that their destruction through oxidative mechanisms normally exerted by myeloid cells, such as neutrophils and eosinophils, or their persistence in the setting of pathologic extracellular reducing environments, maintained by exuberant necrotic cell death and/or oxidoreductases, represent important molecular means enabling chronic inflammatory states.