Evidence map›Paper›PMID 42231135›Full record

ReviewProtein science : a publication of the Protein Society2026

Redox signals and oxidative stress in the control of mitochondrial protein import.

Lidwina Hasberg, Viktoria Katharina Lauterbach, Torsten Ochsenreiter, Jan Riemer

Abstract readReview
In one paragraph

Review in Protein science : a publication of the Protein Society, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. Redox signals and oxidative stress in the control of mitochondrial protein import.Protein science : a publication of the Protein Society · 2026
    Review
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.

Lidwina HasbergRedox Metabolism Group, Institute for Biochemistry, Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), and Center for Molecular Medicine (CMMC), University of Cologne, Cologne, Germany.
Viktoria Katharina LauterbachRedox Metabolism Group, Institute for Biochemistry, Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), and Center for Molecular Medicine (CMMC), University of Cologne, Cologne, Germany.
Torsten OchsenreiterInstitute of Cell Biology, University of Bern, Bern, Switzerland.
Jan RiemerRedox Metabolism Group, Institute for Biochemistry, Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD), and Center for Molecular Medicine (CMMC), University of Cologne, Cologne, Germany.ORCID 0000-0002-7574-8457

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondrial protein import is essential for organelle biogenesis and cellular homeostasis. It operates in an environment that is intrinsically shaped by redox chemistry. Mitochondria are major sources of reactive oxygen species (ROS), which arise as by-products of oxidative phosphorylation. Cells therefore maintain sophisticated ROS-handling systems, including compartmentalized antioxidant networks, to balance redox signaling with protection from oxidative stress. Increasing evidence indicates that these redox conditions directly influence mitochondrial protein import at multiple levels. In this review, we provide an overview of ROS production, ROS signaling, and oxidative stress in relation to mitochondrial protein import. We outline the major mitochondrial protein import pathways, and discuss how their activity is modulated by redox-dependent mechanisms. A particular focus is placed on the mitochondrial disulfide relay system of the intermembrane space, which directly couples protein import to redox chemistry through oxidative folding, and how it is influenced by the local redox environment. Collectively, we propose that mitochondrial protein import is partially governed by redox-dependent mechanisms, enabling integration of metabolic state, stress responses, and signaling pathways.

Indexed as

MitochondriaMitochondrial ProteinsOxidative StressSignal TransductionAnimalsHumansOxidation-ReductionProtein TransportReactive Oxygen SpeciesMitochondrial ProteinsReactive Oxygen Speciesdisulfide relaymitochondrial protein importoxidative stressreactive oxygen species (ROS)redox signaling

Identifiers

PMID42231135
PMCPMC13239934

What OpenQuestion holds

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LicenceCC BY
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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.