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Mitochondrial cross-compartmental signalling to maintain proteostasis and longevity. / Molenaars, Marte; Daniels, Eileen G.; Meurs, Amber et al.

In: Philosophical transactions of the Royal Society of London. Series B, Biological sciences, Vol. 375, No. 1801, 20190414, 22.06.2020, p. 20190414.

Research output: Contribution to journalReview articleAcademicpeer-review

Harvard

Molenaars, M, Daniels, EG, Meurs, A, Janssens, GE & Houtkooper, RH 2020, 'Mitochondrial cross-compartmental signalling to maintain proteostasis and longevity', Philosophical transactions of the Royal Society of London. Series B, Biological sciences, vol. 375, no. 1801, 20190414, pp. 20190414. https://doi.org/10.1098/rstb.2019.0414, https://doi.org/10.1098/rstb.2019.0414

APA

Vancouver

Molenaars M, Daniels EG, Meurs A, Janssens GE, Houtkooper RH. Mitochondrial cross-compartmental signalling to maintain proteostasis and longevity. Philosophical transactions of the Royal Society of London. Series B, Biological sciences. 2020 Jun 22;375(1801):20190414. 20190414. https://doi.org/10.1098/rstb.2019.0414, https://doi.org/10.1098/rstb.2019.0414

Author

Molenaars, Marte ; Daniels, Eileen G. ; Meurs, Amber et al. / Mitochondrial cross-compartmental signalling to maintain proteostasis and longevity. In: Philosophical transactions of the Royal Society of London. Series B, Biological sciences. 2020 ; Vol. 375, No. 1801. pp. 20190414.

BibTeX

@article{0f7f1c919cf045dbb1774abc46118906,
title = "Mitochondrial cross-compartmental signalling to maintain proteostasis and longevity",
abstract = "Lifespan in eukaryotic species can be prolonged by shifting from cellular states favouring growth to those favouring maintenance and stress resistance. For instance, perturbations in mitochondrial oxidative phosphorylation (OXPHOS) can shift cells into this latter state and extend lifespan. Because mitochondria rely on proteins synthesized from nuclear as well as mitochondrial DNA, they need to constantly send and receive messages from other compartments of the cell in order to function properly and maintain homeostasis, and lifespan extension is often dependent on this cross-compartmental signalling. Here, we describe the mechanisms of bi-directional mitochondrial cross-compartmental signalling resulting in proteostasis and longevity. These proteostasis mechanisms are highly context-dependent, governed by the origin and extent of stress. Furthermore, we discuss the translatability of these mechanisms and explore therapeutic developments, such as the antibiotic studies targeting mitochondria or mitochondria-derived peptides as therapies for age-related diseases such as neurodegeneration and cancer. This article is part of the theme issue {\textquoteleft}Retrograde signalling from endosymbiotic organelles{\textquoteright}.",
keywords = "Longevity, Mitochondria, Proteostasis, Retrograde signalling",
author = "Marte Molenaars and Daniels, {Eileen G.} and Amber Meurs and Janssens, {Georges E.} and Houtkooper, {Riekelt H.}",
year = "2020",
month = jun,
day = "22",
doi = "10.1098/rstb.2019.0414",
language = "English",
volume = "375",
pages = "20190414",
journal = "Philosophical transactions of the Royal Society of London. Series B, Biological sciences",
issn = "0962-8436",
publisher = "Royal Society of London",
number = "1801",

}

RIS

TY - JOUR

T1 - Mitochondrial cross-compartmental signalling to maintain proteostasis and longevity

AU - Molenaars, Marte

AU - Daniels, Eileen G.

AU - Meurs, Amber

AU - Janssens, Georges E.

AU - Houtkooper, Riekelt H.

PY - 2020/6/22

Y1 - 2020/6/22

N2 - Lifespan in eukaryotic species can be prolonged by shifting from cellular states favouring growth to those favouring maintenance and stress resistance. For instance, perturbations in mitochondrial oxidative phosphorylation (OXPHOS) can shift cells into this latter state and extend lifespan. Because mitochondria rely on proteins synthesized from nuclear as well as mitochondrial DNA, they need to constantly send and receive messages from other compartments of the cell in order to function properly and maintain homeostasis, and lifespan extension is often dependent on this cross-compartmental signalling. Here, we describe the mechanisms of bi-directional mitochondrial cross-compartmental signalling resulting in proteostasis and longevity. These proteostasis mechanisms are highly context-dependent, governed by the origin and extent of stress. Furthermore, we discuss the translatability of these mechanisms and explore therapeutic developments, such as the antibiotic studies targeting mitochondria or mitochondria-derived peptides as therapies for age-related diseases such as neurodegeneration and cancer. This article is part of the theme issue ‘Retrograde signalling from endosymbiotic organelles’.

AB - Lifespan in eukaryotic species can be prolonged by shifting from cellular states favouring growth to those favouring maintenance and stress resistance. For instance, perturbations in mitochondrial oxidative phosphorylation (OXPHOS) can shift cells into this latter state and extend lifespan. Because mitochondria rely on proteins synthesized from nuclear as well as mitochondrial DNA, they need to constantly send and receive messages from other compartments of the cell in order to function properly and maintain homeostasis, and lifespan extension is often dependent on this cross-compartmental signalling. Here, we describe the mechanisms of bi-directional mitochondrial cross-compartmental signalling resulting in proteostasis and longevity. These proteostasis mechanisms are highly context-dependent, governed by the origin and extent of stress. Furthermore, we discuss the translatability of these mechanisms and explore therapeutic developments, such as the antibiotic studies targeting mitochondria or mitochondria-derived peptides as therapies for age-related diseases such as neurodegeneration and cancer. This article is part of the theme issue ‘Retrograde signalling from endosymbiotic organelles’.

KW - Longevity

KW - Mitochondria

KW - Proteostasis

KW - Retrograde signalling

UR - http://www.scopus.com/inward/record.url?scp=85085082705&partnerID=8YFLogxK

U2 - 10.1098/rstb.2019.0414

DO - 10.1098/rstb.2019.0414

M3 - Review article

C2 - 32362258

VL - 375

SP - 20190414

JO - Philosophical transactions of the Royal Society of London. Series B, Biological sciences

JF - Philosophical transactions of the Royal Society of London. Series B, Biological sciences

SN - 0962-8436

IS - 1801

M1 - 20190414

ER -

ID: 11684267