Evidence map›Paper›PMID 40120684›Full record

ArticleThe Journal of biological chemistry2025

H

David A Hanna, Brandon Chen, Yatrik M Shah, Oleh Khalimonchuk, Brian Cunniff, Ruma Banerjee

Abstract read
In one paragraph

Article in The Journal of biological chemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
–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

9 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. The microbiota-proteostasis axis: implications in neurodegenerative diseases.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026
    Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Review
  9. Review
4 · The record

Corrections and comments

  • Update of
    H2024
5 · Who and what money

Authors and funding

6 authors.

David A HannaDepartment of Biological Chemistry, Michigan Medicine, Ann Arbor, Michigan, USA.
Brandon ChenDepartment of Molecular and Integrative Physiology, Michigan Medicine, Ann Arbor, Michigan, USA; Department of Cellular and Molecular Biology Program, Michigan Medicine, Ann Arbor, Michigan, USA.
Yatrik M ShahDepartment of Molecular and Integrative Physiology, Michigan Medicine, Ann Arbor, Michigan, USA; Department of internal Medicine (Division of Gastroenterology), Michigan Medicine, Ann Arbor, Michigan, USA.
Oleh KhalimonchukDepartment of Biochemistry, University of Nebraska-Lincoln, Lincoln, Nebraska, USA.
Brian CunniffDepartment of Pathology and Laboratory Medicine, University of Vermont Larner College of Medicine, Burlington, Vermont, USA.
Ruma BanerjeeDepartment of Biological Chemistry, Michigan Medicine, Ann Arbor, Michigan, USA. Electronic address: rbanerje@umich.edu.

Funding

Sulfide Oxidation and SignalingR35GM130183 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI RUMA V BANERJEE · 2019 to 2026
$3.6M
Mitochondrial Fidelity and HomeostasisR35GM131701 · NIGMS · UNIVERSITY OF NEBRASKA LINCOLN · PI Oleh Khalimonchuk · 2019 to 2026
$2.4M
Mitochondrial positioning regulates redox-signaling during cell migrationR01GM143250 · NIGMS · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI Brian Cunniff · 2023 to 2026
$1.3M
Sulfide metabolism at the host microbiome interfaceF32GM140694 · NIGMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI HANNA, DAVID A · 2021 to 2023
$205k
NIGMS NIH HHS F32 GM140694NIGMS NIH HHS R01 GM143250NIGMS NIH HHS R35 GM130183NIGMS NIH HHS R35 GM131701
6 · The paper itself

Abstract

Mitochondrial form and function are intimately interconnected, responding to cellular stresses and changes in energy demand. Hydrogen sulfide, a product of amino acid metabolism, has dual roles as an electron transport chain substrate and complex IV (CIV) inhibitor, leading to a reductive shift, which has pleiotropic metabolic consequences. Luminal sulfide concentration in the colon is high due to microbial activity, and in this study, we demonstrate that chronic sulfide exposure of colonocyte-derived cells leads to lower Mic60 and Mic19 expression that is correlated with a profound loss of cristae and lower mitochondrial networking. Sulfide-induced depolarization of the inner mitochondrial membrane activates Oma1-dependent cleavage of Opa1 and is associated with a profound loss of CI and CIV activities associated with respirasomes. Our study reveals a potential role for sulfide as an endogenous modulator of mitochondrial dynamics and suggests that this regulation is corrupted in hereditary or acquired diseases associated with elevated sulfide.

Indexed as

Electron Transport Complex IVHydrogen SulfideMitochondriaAnimalsGTP PhosphohydrolasesHumansMiceMitochondrial DynamicsMitochondrial ProteinsElectron Transport Complex IVGTP PhosphohydrolasesHydrogen SulfideMitochondrial Proteinscristaeelectron transport chainhydrogen sulfidemitochondrial dynamicsrespirasome

Identifiers

PMID40120684
PMCPMC12022479

What Socratic 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 Socratic graph.