Published May 2018 | Version v1
Journal article

Mitochondrial adventures at the organelle society

  • 1. Universitätsmedizin Göttingen, Institute fur Zellbiochemie, Humboldtallee 23, room 01.423, 37073 Göttingen (Germany)
  • 2. International Max-Planck Research School in Neuroscience, Göttingen (Germany)

Description

Highlights: • Mitochondrial malfunction affects lysosomal biogenesis via AMPK signaling. • Lysosomal malfunction represses mitochondrial function. • ER stress promotes degradation of damaged mitochondria. • Organelle crosstalk is a key component of mitochondrial signaling in physiology and pathology. Mitochondria are constantly communicating with the rest of the cell. Defects in mitochondria underlie severe pathologies, whose mechanisms remain poorly understood. It is becoming increasingly evident that mitochondrial malfunction resonates in other organelles, perturbing their function and their biogenesis. In this manuscript, we review the current knowledge on the cross-talk between mitochondria and other organelles, particularly lysosomes, peroxisomes and the endoplasmic reticulum. Several organelle interactions are mediated by transcriptional programs, and other signaling mechanisms are likely mediating organelle dysfunction downstream of mitochondrial impairments. Many of these organelle crosstalk pathways are likely to have a role in pathological processes.

Availability note (English)

Available from http://dx.doi.org/10.1016/j.bbrc.2017.04.124

Additional details

Identifiers

DOI
10.1016/j.bbrc.2017.04.124;
PII
S0006291X17308069;

Publishing Information

Journal Title
Biochemical and Biophysical Research Communications
Journal Volume
500
Journal Issue
1
Journal Page Range
p. 87-93
ISSN
0006-291X
CODEN
BBRCA9

INIS

Country of Publication
United States
Country of Input or Organization
International Atomic Energy Agency (IAEA)
INIS RN
53054364
Subject category
S60: APPLIED LIFE SCIENCES;
Descriptors DEI
ENDOPLASMIC RETICULUM; LYSOSOMES; MITOCHONDRIA; SIGNALS; STRESSES
Descriptors DEC
CELL CONSTITUENTS

Optional Information

Copyright
Copyright (c) 2017 The Authors. Published by Elsevier Inc.