Paolo Grumati

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: 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: Severe disruption of Fam134b in mice causes expansion of the ER, inhibits ER turnover, sensitizes cells to stress-induced apoptotic cell death and leads to degeneration of sensory neurons, so selective ER-phagy via FAM134 proteins is indispensable for mammalian cell homeostasis and controls ER morphology and turnover in mice and humans.

TL;DR: Force activation of autophagy by genetic, dietary and pharmacological approaches restored myofiber survival and ameliorated the dystrophic phenotype of Col6a1−/− mice, indicating that defective activation of the autophagic machinery is pathogenic in some congenital muscular dystrophies.

TL;DR: It is shown that the extracellular matrix protein collagen VI is a key component of the satellite cell niche and establishes a critical role for an extracllular matrix molecule in satellite cell self-renewal and open new venues for therapies of collagen VI-related muscle diseases.