Mitochondrial adventures at the organelle society
Creators
- 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.2017.04.124Additional 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.