Evidence map›Paper›PMID 41026942›Full record

ReviewClinical science (London, England : 1979)2025

Double-edged mitophagy: balancing inflammation and resolution in lung disease.

Sijia Tian, Yingyi Zhang, Chuanchuan Liu, Huajing Zhang, Qianying Lu, Yanmei Zhao, Haojun Fan

Abstract readReview
In one paragraph

Review in Clinical science (London, England : 1979), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed.

  1. Review
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  5. Cisplatin-Induced Nephrotoxicity Attenuation byInternational journal of molecular sciences · 2026
    Article
  6. Article
  7. Article
  8. Roles of mitophagy and immune infiltration in Parkinson's disease: new perspectives from bioinformatics analysis and A53T transgenic mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  9. [The role and mechanism of chemokine network in promoting osteoarthritis progression by regulating synovial macrophage heterogeneity].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2026
    Review
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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

7 authors.

Sijia Tian *School of Disaster and Emergency Medicine, Tianjin University, 300072, China.ORCID 0009-0009-5635-7942
Yingyi Zhang *School of Disaster and Emergency Medicine, Tianjin University, 300072, China.ORCID 0000-0003-1020-7964
Chuanchuan Liu *School of Disaster and Emergency Medicine, Tianjin University, 300072, China.ORCID 0009-0000-9841-6570
Huajing ZhangSchool of Disaster and Emergency Medicine, Tianjin University, 300072, China.
Qianying LuSchool of Disaster and Emergency Medicine, Tianjin University, 300072, China.ORCID 0000-0002-0810-4483
Yanmei ZhaoSchool of Disaster and Emergency Medicine, Tianjin University, 300072, China.ORCID 0000-0002-8572-6470
Haojun FanSchool of Disaster and Emergency Medicine, Tianjin University, 300072, China.ORCID 0000-0003-1111-0232

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammatory lung diseases, such as chronic obstructive pulmonary disease (COPD), acute lung injury (ALI)/acute respiratory distress syndrome (ARDS), and asthma, are driven by mitochondrial dysfunction and aberrant immune responses, yet the regulatory role of mitophagy-a selective autophagy eliminating damaged mitochondria-remains poorly defined. This review synthesizes evidence from in vivo and in vitro studies to dissect the molecular interplay between mitophagy and inflammation. Key fundings reveal that mitophagy exerts context-dependent effects: Protective mitophagy (via PTEN-induced putative kinase 1 [PINK1]-Parkin or FUN14 domain-containing protein 1 [FUNDC1] pathways) clears mitochondrial reactive oxygen species (mtROS)/mitochondrial DNA (mtDNA), suppressing NOD-like receptor thermal protein domain associated protein 3 (NLRP3) inflammasome activation and pyroptosis, but excessive mitophagy exacerbates mitochondrial fragmentation and necroptosis. Notably, bidirectional cross-talk exists, and therapeutic strategies-genetic and pharmacological-could restore mitophagy flux, attenuating inflammation in preclinical models. However, challenges persist in targeting tissue-specific mitophagy (such as alveolar and bronchial epithelia). This work underscores mitophagy as a double-edged sword in lung inflammation and proposes precision interventions to balance mitochondrial quality control, offering novel avenues for inflammatory lung diseases.

Indexed as

InflammationLung DiseasesMitochondriaMitophagyAnimalsHumansInflammasomesInflammasomesinflammationlung diseasesmitophagymtROStherapeutic targeting

Identifiers

PMID41026942
PMCPMC12599259

What OpenQuestion holds

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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.