Cited by 57Cancer, Hypoxia, and MetabolismRNA and protein synthesis mechanismsPI3K/AKT/mTOR signaling in cancer

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Cellular oxygen sensing, signalling and how to survive translational arrest in hypoxia

Fähling, M.·2009·Acta Physiologica

DOI 10.1111/j.1748-1716.2008.01894.x

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Abstract

Hypoxia is a consequence of inadequate oxygen availability. At the cellular level, lowered oxygen concentration activates signal cascades including numerous receptors, ion channels, second messengers, as well as several protein kinases and phosphatases. This, in turn, activates trans‐factors like transcription factors, RNA‐binding proteins and miRNAs, mediating an alteration in gene expression control. Each cell type has its unique constellation of oxygen sensors, couplers and effectors that determine the activation and predominance of several independent hypoxia‐sensitive pathways. Hence, altered gene expression patterns in hypoxia result from a complex regulatory network with multiple divergences and convergences. Although hundreds of genes are activated by transcriptional control in hypoxia, metabolic rate depression, as a consequence of reduced ATP level, causes inhibition of mRNA translation. In a multi‐phase response to hypoxia, global protein synthesis is suppressed, mainly by phosphorylation of eIF2‐alpha by PERK and inhibition of mTOR, causing suppression of 5′‐cap‐dependent mRNA translation. Growing evidence suggests that mRNAs undergo sorting at stress granules, which determines the fate of mRNA as to whether being translated, stored, or degraded. Data indicate that translation is suppressed only at ‘free’ polysomes, but is active at subsets of membrane‐bound ribosomes. The recruitment of specific mRNAs into subcellular compartments seems to be crucial for local mRNA translation in prolonged hypoxia. Furthermore, ribosomes themselves may play a significant role in targeting mRNAs for translation. This review summarizes the multiple facets of the cellular adaptation to hypoxia observed in mammals.

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Authors: Fähling, M.
Affiliations: Charité – Universitätsmedizin Berlin (DE)
Corresponding author: Fähling, M.
ORCID: Fähling, M.
Venue: Acta Physiologica
Publisher: Wiley
Published: 2009-01-05
Volume: 195
Issue: 2
Pages: 205-230
ISSN: 1748-1708 (ISSN-L)
1748-1716
DOI: 10.1111/j.1748-1716.2008.01894.x
OpenAlex: W2065309438
Cited by: 57
References: 283
Citations by year: 2026: 1 · 2025: 2 · 2024: 1 · 2023: 2 · 2021: 1 · 2020: 2 · 2019: 3 · 2018: 2 · 2017: 5 · 2016: 6 · 2015: 2 · 2014: 2 · 2013: 8 · 2012: 5
FWCI: 0.36
Type: journal article
Language: en
Open access: closed
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations: Acta Physiologica (publishedVersion)
PubMed (publishedVersion)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Hypoxia, and Metabolism
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA and protein synthesis mechanisms
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
Keywords: hypoxia, cellular oxygen sensing, hypoxia signaling, translational arrest, eIF2α phosphorylation, PERK, mTOR inhibition, stress granules, mRNA translation, membrane-bound ribosomes, local translation, transcriptional regulation, gene expression regulation
MeSH terms: Adenosine Triphosphate, Animals, Calcium, Cells, Gene Expression Regulation, Humans, Mammals, Oxygen, Ribosomes, Protein Biosynthesis, Cell Hypoxia, Reactive Oxygen Species, Reactive Nitrogen Species

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Cellular oxygen sensing, signalling and how to survive translational arrest in hypoxia

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