Mitochondrial function — gatekeeper of intestinal epithelial cell homeostasis DOI
Eva Rath, Antonio Moschetta, Dirk Haller

et al.

Nature Reviews Gastroenterology & Hepatology, Journal Year: 2018, Volume and Issue: 15(8), P. 497 - 516

Published: May 29, 2018

Language: Английский

Mitophagy and Quality Control Mechanisms in Mitochondrial Maintenance DOI Creative Commons
Sarah Pickles,

Pierre Vigié,

Richard J. Youle

et al.

Current Biology, Journal Year: 2018, Volume and Issue: 28(4), P. R170 - R185

Published: Feb. 1, 2018

Language: Английский

Citations

1620
Cellular adaptation to hypoxia through hypoxia inducible factors and beyond DOI
Pearl Lee, Navdeep S. Chandel, M. Celeste Simon

et al.

Nature Reviews Molecular Cell Biology, Journal Year: 2020, Volume and Issue: 21(5), P. 268 - 283

Published: March 6, 2020

Language: Английский

Citations

897
Endoplasmic reticulum stress signalling – from basic mechanisms to clinical applications DOI Creative Commons

Aitor Almanza,

Antonio Carlesso, Chetan Chintha

et al.

FEBS Journal, Journal Year: 2018, Volume and Issue: 286(2), P. 241 - 278

Published: July 20, 2018

The endoplasmic reticulum (ER) is a membranous intracellular organelle and the first compartment of secretory pathway. As such, ER contributes to production folding approximately one-third cellular proteins, thus inextricably linked maintenance homeostasis fine balance between health disease. Specific stress signalling pathways, collectively known as unfolded protein response (UPR), are required for maintaining homeostasis. UPR triggered when capacity overwhelmed by demand initially aims restore normal functions. However, if this fails, then triggers cell death. In review, we provide signalling-centric view functions, from ER's discovery latest advancements in understanding biology. Our review provides synthesis revolving around proteostasis UPR, its impact on other organelles behaviour, multifaceted dynamic role physiology, before finally exploring potential exploitation knowledge tackle unresolved biological questions address unmet biomedical needs. Thus, an integrated global existing literature pathways their use therapeutic purposes.

Language: Английский

Citations

819
Enhancing mitochondrial proteostasis reduces amyloid-β proteotoxicity DOI
Vincenzo Sorrentino, Mario Romani,

Laurent Mouchiroud

et al.

Nature, Journal Year: 2017, Volume and Issue: 552(7684), P. 187 - 193

Published: Dec. 1, 2017

Language: Английский

Citations

565
The mitochondrial UPR: mechanisms, physiological functions and implications in ageing DOI
Tomer Shpilka, Cole M. Haynes

Nature Reviews Molecular Cell Biology, Journal Year: 2017, Volume and Issue: 19(2), P. 109 - 120

Published: Nov. 22, 2017

Language: Английский

Citations

562
Mitochondrial stress is relayed to the cytosol by an OMA1–DELE1–HRI pathway DOI
Xiaoyan Guo, Giovanni Aviles, Yi Liu

et al.

Nature, Journal Year: 2020, Volume and Issue: 579(7799), P. 427 - 432

Published: March 4, 2020

Language: Английский

Citations

490
UPRmt regulation and output: a stress response mediated by mitochondrial-nuclear communication DOI Creative Commons

Andrew Melber,

Cole M. Haynes

Cell Research, Journal Year: 2018, Volume and Issue: 28(3), P. 281 - 295

Published: Feb. 9, 2018

The mitochondrial network is not only required for the production of energy, essential cofactors and amino acids, but also serves as a signaling hub innate immune apoptotic pathways. Multiple mechanisms have evolved to identify combat dysfunction maintain health organism. One such pathway unfolded protein response (UPR

Language: Английский

Citations

426
Base-Resolution Mapping Reveals Distinct m1A Methylome in Nuclear- and Mitochondrial-Encoded Transcripts DOI Creative Commons
Xiaoyu Li, Xushen Xiong, Meiling Zhang

et al.

Molecular Cell, Journal Year: 2017, Volume and Issue: 68(5), P. 993 - 1005.e9

Published: Nov. 5, 2017

Language: Английский

Citations

419
The gut microbiota influences skeletal muscle mass and function in mice DOI Open Access
Shawon Lahiri, Hye-Jin Kim, Isabel García‐Pérez

et al.

Science Translational Medicine, Journal Year: 2019, Volume and Issue: 11(502)

Published: July 24, 2019

Transplanting the gut microbiota of pathogen-free mice into germ-free improves skeletal muscle mass and strength.

Language: Английский

Citations

405
Regulation of Nrf2 by Mitochondrial Reactive Oxygen Species in Physiology and Pathology DOI Creative Commons
Shuya Kasai, Sunao Shimizu, Yota Tatara

et al.

Biomolecules, Journal Year: 2020, Volume and Issue: 10(2), P. 320 - 320

Published: Feb. 17, 2020

Reactive oxygen species (ROS) are byproducts of aerobic respiration and signaling molecules that control various cellular functions. Nrf2 governs the gene expression endogenous antioxidant synthesis ROS-eliminating enzymes in response to electrophilic compounds inactivate negative regulator Keap1. Accumulating evidence has shown mitochondrial ROS (mtROS) activate Nrf2, often mediated by certain protein kinases, induce genes involved quality/quantity control. Mild physiological stress, such as caloric restriction exercise, elicits beneficial effects through a process known "mitohormesis." Exercise induces NOX4 heart, which activates increases endurance capacity. Mice transiently depleted SOD2 or overexpressing skeletal muscle-specific UCP1 exhibit Nrf2-mediated PGC1α-mediated biogenesis. ATF4 activation may transcriptional program enhances NADPH mitochondria might cooperate with system. In severe oxidative Klf9 expression, represses mtROS-eliminating enhance cell death. is inactivated pathological conditions, diabetes, but Keap1 down-regulation mtROS elimination rescues improves pathology. These reports aid us understanding roles pathophysiological alterations involving mtROS.

Language: Английский

Citations

402