Contents

May 2020
Vol 6, Issue 19

About The Cover

Cover image expansion

ONLINE COVER Although scientists have been aware that miscommunication between the endoplasmic reticulum (which synthesizes proteins and lipids) and the mitochondria (which generates cell power) occurs in a number of degenerative and inflammatory-related diseases, it has remained unclear whether this disrupted crosstalk occurs in cystic fibrosis, a disease that damages the lungs and digestive system. Scientists have also been unsure whether calcium ion signaling, and autophagy are directly related to the pathogenic cascade that occurs in the lungs during cystic fibrosis. To better understand the mechanisms behind this disease, Rimessi et al. exposed different human bronchial cell models to P. aeruginosa, the bacterial agent of cystic fibrosis lung infections, from the airways of patients, finding an increase in interactions between cells from the endoplasmic reticulum and mitochondria. They also exposed bronchial cells from patients with and without the disease to the bacteria for multiple hours, finding an increase in the expression of endoplasmic reticulum-mitochondria tethers in cells from patients with cystic fibrosis. Rimessi et al. found they could alleviate inflammatory response by inhibiting a mitochondrial calcium uniporter, resulting in a potential therapeutic strategy. [CREDIT: PHOTOSTOCK-ISRAEL/SCIENCE SOURCE]