Evidence map›Paper›PMID 31547228›Full record

ReviewCells2019

Mechanistic Connections between Endoplasmic Reticulum (ER) Redox Control and Mitochondrial Metabolism.

Yuxiang Fan, Thomas Simmen

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed, 1 pooled it
7.4field-weighted citation impact, top 2% 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

82 citing papers in PubMed, 1 synthesis or guideline pooled it, 140 citations in OpenAlex.

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  19. Cytosine methylase and hydroxymethylase activity in mammalian mitochondria.Frontiers in cell and developmental biology · 2025
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22 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 2 countries.

Yuxiang FanDepartment of Cell Biology, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, AB T6G2H7, Canada. yuxiang@ualberta.ca.
Thomas SimmenDepartment of Cell Biology, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, AB T6G2H7, Canada. tsimmen@ualberta.ca.ORCID 0000-0002-2350-2965
University of Alberta · CA

Funding

CIHR PS162449
6 · The paper itself

Abstract

The past decade has seen the emergence of endoplasmic reticulum (ER) chaperones as key determinants of contact formation between mitochondria and the ER on the mitochondria-associated membrane (MAM). Despite the known roles of ER-mitochondria tethering factors like PACS-2 and mitofusin-2, it is not yet entirely clear how they mechanistically interact with the ER environment to determine mitochondrial metabolism. In this article, we review the mechanisms used to communicate ER redox and folding conditions to the mitochondria, presumably with the goal of controlling mitochondrial metabolism at the Krebs cycle and at the electron transport chain, leading to oxidative phosphorylation (OXPHOS). To achieve this goal, redox nanodomains in the ER and the interorganellar cleft influence the activities of ER chaperones and Ca

Indexed as

Oxidation-ReductionAutophagyCalcium SignalingEndoplasmic ReticulumHomeostasisMembrane ProteinsMitochondriaMitochondrial DynamicsMitochondrial MembranesMitochondrial ProteinsMolecular ChaperonesOxidoreductasesMembrane ProteinsMitochondrial ProteinsMolecular ChaperonesOxidoreductasesautophagychaperonesendoplasmic reticulumER-phagymitochondriaredox

Identifiers

PMID31547228
PMCPMC6769559
OpenAlexW2972776431

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.