Ulises Ahumada-Castro

TL;DR: In this article, the authors present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes.

TL;DR: Current evidence for mitochondrial dysfunction caused by Ca2+ miscommunication in neuronal models of neurodegenerative disorders related to aging is looked at, with special emphasis on AD.

TL;DR: It is demonstrated that mitochondria play a fundamental role in maintaining bioenergetic homeostasis of both OXPHOS-competent and OX PHOS-defective cells, with Ca2+ regulation of αKGDH activity playing a pivotal role.

TL;DR: It is proposed that upon ER-mitochondrial Ca2+ transfer inhibition, AMPK present at the mitochondria-associated membranes (MAMs) activate localized autophagy via BECN1 (beclin 1), which could prevent the proper interorganelle communication that would allow the autophile-derived metabolites to reach the necessary anabolic pathways to maintain mitochondrial function and cellular homeostasis.

TL;DR: TNBC cell migration is susceptible to mitochondrial alterations induced by small molecules as FR58P1a, which may have therapeutic implications, and is shown to be a mild uncoupling of OXPHOS.