Evidence map›Paper›PMID 38773615›Full record

ArticleJournal of translational medicine2024

Lactate facilitated mitochondrial fission-derived ROS to promote pulmonary fibrosis via ERK/DRP-1 signaling.

Zhiheng Sun, Zhihua Ji, Huiwen Meng, Wanyu He, Bin Li, Xiaoyue Pan, Yanlin Zhou, Guoying Yu

Abstract read
In one paragraph

Article in Journal of translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing 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

34 citing papers in PubMed.

  1. Article
  2. Advances in metabolic reprogramming of pulmonary fibrosis.Chinese medical journal pulmonary and critical care medicine · 2026
    Review
  3. Article
  4. Article
  5. MCT4 mediates hypoxia-induced extracellular lactate release from IPF fibroblasts.American journal of respiratory cell and molecular biology · 2026
    Article
  6. Article
  7. Pulmonary fibrosis: Emerging targets and novel therapeutics.The Journal of international medical research · 2026
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  20. Ecm19 coordinates mitochondrial fission and cellular redox homeostasis.Redox report : communications in free radical research · 2025
    Article
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

8 authors.

Zhiheng SunCollege of Life Science, Institute of Biomedical Science, Henan Normal University, Xinxiang, Henan, China. sunzhiheng@htu.edu.cn.ORCID 0000-0001-5462-9689
Zhihua JiCollege of Life Science, Institute of Biomedical Science, Henan Normal University, Xinxiang, Henan, China.
Huiwen MengCollege of Life Science, Institute of Biomedical Science, Henan Normal University, Xinxiang, Henan, China.
Wanyu HeCollege of Life Science, Institute of Biomedical Science, Henan Normal University, Xinxiang, Henan, China.
Bin LiCollege of Life Science, Institute of Biomedical Science, Henan Normal University, Xinxiang, Henan, China.
Xiaoyue PanCollege of Life Science, Institute of Biomedical Science, Henan Normal University, Xinxiang, Henan, China.
Yanlin ZhouCollege of Life Science, Institute of Biomedical Science, Henan Normal University, Xinxiang, Henan, China.
Guoying YuCollege of Life Science, Institute of Biomedical Science, Henan Normal University, Xinxiang, Henan, China. guoyingyu@htu.edu.cn.

Funding

Henan Normal University Research Launch Foundation 20220099Ministry of Science and Technology 2019YFE0119500National Natural Science Foundation youth fund of China 32200714
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, fibrotic interstitial lung diseases, which mainly existed in middle-aged and elderly people. The accumulation of reactive oxygen species (ROS) is a common characteristic of IPF. Previous research also shown that lactate levels can be abnormally elevated in IPF patients. Emerging evidence suggested a relationship between lactate and ROS in IPF which needs further elucidation. In this article, we utilized a mouse model of BLM-induced pulmonary fibrosis to detect alterations in ROS levels and other indicators associated with fibrosis. Lactate could induce mitochondrial fragmentation by modulating expression and activity of DRP1 and ERK. Moreover, Increased ROS promoted P65 translocation into nucleus, leading to expression of lung fibrotic markers. Finally, Ulixertinib, Mdivi-1 and Mito-TEMPO, which were inhibitor activity of ERK, DRP1 and mtROS, respectively, could effectively prevented mitochondrial damage and production of ROS and eventually alleviate pulmonary fibrosis. Taken together, these findings suggested that lactate could promote lung fibrosis by increasing mitochondrial fission-derived ROS via ERK/DRP1 signaling, which may provide novel therapeutic solutions for IPF.

Indexed as

DynaminsMice, Inbred C57BLMitochondrial DynamicsReactive Oxygen SpeciesAnimalsBleomycinExtracellular Signal-Regulated MAP KinasesHumansLactic AcidMaleMAP Kinase Signaling SystemMiceMitochondriaPulmonary FibrosisSignal TransductionBleomycinDnm1l protein, mouseDynaminsExtracellular Signal-Regulated MAP KinasesLactic AcidReactive Oxygen SpeciesDRP1Idiopathic pulmonary fibrosisLactateMitochondrial fissionReactive oxygen species

Identifiers

PMID38773615
PMCPMC11106888

What OpenQuestion holds

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Registered trials

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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.