Evidence map›Paper›PMID 37603398›Full record

ReviewBioEssays : news and reviews in molecular, cellular and developmental biology2023

The evolution of selective autophagy as a mechanism of oxidative stress response: The evolutionarily acquired ability of selective autophagy receptors to respond to oxidative stress is beneficial for human longevity.

Joshua Ratliffe, Tetsushi Kataura, Elsje G Otten, Viktor I Korolchuk

Open access · hybridAbstract readReview
In one paragraph

Review in BioEssays : news and reviews in molecular, cellular and developmental biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.7field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 8 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Joshua RatliffeBiosciences Institute, Faculty of Medical Sciences, Newcastle University, Newcastle upon Tyne, UK.
Tetsushi KatauraBiosciences Institute, Faculty of Medical Sciences, Newcastle University, Newcastle upon Tyne, UK.
Elsje G OttenBiosciences Institute, Faculty of Medical Sciences, Newcastle University, Newcastle upon Tyne, UK.
Viktor I KorolchukBiosciences Institute, Faculty of Medical Sciences, Newcastle University, Newcastle upon Tyne, UK.
Newcastle University · GB

Funding

BBSRC BB/M023389/1BBSRC BB/R008167/2EPSRC PhD studentship EP/W524700/1The International Medical Research FoundationUehara Memorial Foundation
6 · The paper itself

Abstract

Ageing is associated with a decline in autophagy and elevated reactive oxygen species (ROS), which can breach the capacity of antioxidant systems. Resulting oxidative stress can cause further cellular damage, including DNA breaks and protein misfolding. This poses a challenge for longevous organisms, including humans. In this review, we hypothesise that in the course of human evolution selective autophagy receptors (SARs) acquired the ability to sense and respond to localised oxidative stress. We posit that in the vicinity of protein aggregates and dysfunctional mitochondria oxidation of key cysteine residues in SARs induces their oligomerisation which initiates autophagy. The degradation of damaged cellular components thus could reduce ROS production and restore redox homeostasis. This evolutionarily acquired function of SARs may represent one of the biological adaptations that contributed to longer lifespan. Inversely, loss of this mechanism can lead to age-related diseases associated with impaired autophagy and oxidative stress.

Indexed as

AutophagyLongevityOxidative StressReactive Oxygen SpeciesAgingAnimalsBiological EvolutionHumansMitochondriaOxidation-ReductionReactive Oxygen Speciesageingaggrephagyautophagymitophagyneurodegenerationoxidative stressselective autophagy receptors

Identifiers

PMID37603398
PMCPMC11475373
OpenAlexW4386019098

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.