Evidence map›Paper›PMID 29165426›Full record

ReviewNature reviews. Molecular cell biology2018

The mitochondrial UPR: mechanisms, physiological functions and implications in ageing.

Tomer Shpilka, Cole M Haynes

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Molecular cell biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 459 papers.

0numbers the graph read from it
0cells of the map it votes in
459citing papers in PubMed
19.4field-weighted citation impact, top 1% 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

459 citing papers in PubMed, 682 citations in OpenAlex.

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  6. More than the 'master regulator of cytosolic proteostasis': new roles for HSF1 in promoting tissue health.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026
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399 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Tomer ShpilkaDepartment of Molecular, Cell and Cancer Biology, University of Massachusetts Medical School, Worcester, Massachusetts 01655, USA.
Cole M HaynesDepartment of Molecular, Cell and Cancer Biology, University of Massachusetts Medical School, Worcester, Massachusetts 01655, USA.
University of Massachusetts Chan Medical School · US

Funding

MAINTENANCE OF MITOCHONDRIAL PROTEIN FOLDING AS AN AGING EFFECTORR01AG040061 · NIA · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI HAYNES, COLE M · 2011 to 2020
$3.6M
Coordinated Repair and Regeneration of Defective MitochondriaR01AG047182 · NIA · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI HAYNES, COLE M · 2015 to 2019
$2.1M
6 · The paper itself

Abstract

Mitochondrial function declines during ageing owing to the accumulation of deleterious mitochondrial genomes and damage resulting from the localized generation of reactive oxygen species, both of which are often exacerbated in diseases such as Parkinson disease. Cells have several mechanisms to assess mitochondrial function and activate a transcriptional response known as the mitochondrial unfolded protein response (UPR

Indexed as

AgingAnimalsDNA, MitochondrialHumansMitochondriaMitochondrial DiseasesMitochondrial ProteinsMutationParkinson DiseaseReactive Oxygen SpeciesSignal TransductionUnfolded Protein ResponseDNA, MitochondrialMitochondrial ProteinsReactive Oxygen Species

Identifiers

PMID29165426
OpenAlexW2770372563

What OpenQuestion holds

Textmetadata
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.