Evidence map›Paper›PMID 41086860›Full record

ReviewOpen biology2025

HMGB1 and mitochondrial dysfunction: a double-edged sword in ageing.

Maheen Wahid, Margaret Cunningham

Abstract readReview
In one paragraph

Review in Open biology, 2025. 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. 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

2 authors.

Maheen WahidStrathclyde Institute of Pharmacy and Biomedical Sciences, Glasgow, UK.ORCID 0000-0003-1500-0671
Margaret CunninghamStrathclyde Institute of Pharmacy and Biomedical Sciences, Glasgow, UK.

Funding

Scottish Funding CouncilUniversity of Strathclyde
6 · The paper itself

Abstract

Ageing is an intricate and progressive decline across all biological systems, marked by various molecular and cellular processes termed as the hallmarks of ageing. One of the hallmarks is mitochondrial dysfunction, which is brought about through several pathways: mutations in mitochondrial DNA, elevated reactive oxygen species production, disrupted mitochondrial dynamics and impaired mitophagy. Here, we explore the role of high mobility group box 1 (HMGB1) as a potential contributor to mitochondrial dysfunction, examining how it may influence these pathways through its dual roles as both a protector of mitochondrial integrity and a promoter of inflammatory damage. Furthermore, we consider how mitochondrial dysfunction, possibly mediated by HMGB1, could link to other hallmarks of ageing, positioning HMGB1 as a possible central regulator in the ageing process.

Indexed as

AgingHMGB1 ProteinMitochondriaAnimalsDNA, MitochondrialHumansMitophagyReactive Oxygen SpeciesSignal TransductionDNA, MitochondrialHMGB1 ProteinHMGB1 protein, humanReactive Oxygen SpeciesageingHMGB1mitochondrial dysfunction

Identifiers

PMID41086860
PMCPMC12520776

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.