Evidence map›Paper›PMID 38071367›Full record

ArticleNature communications2023

Senescence-associated 13-HODE production promotes age-related liver steatosis by directly inhibiting catalase activity.

Jinjie Duan, Wenhui Dong, Guangyan Wang, Wenjing Xiu, Guangyin Pu, Jingwen Xu, Chenji Ye, Xu Zhang, Yi Zhu, Chunjiong Wang

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
8.4field-weighted citation impact, top 2% of its field
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

27 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Article
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  5. Review
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  7. Article
  8. Kupffer cells: Orchestrators of liver physiology.Liver research (Beijing, China) · 2026
    Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Antioxidants (Basel, Switzerland) · 2025
    Article
  19. Article
  20. 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

10 authors at 2 institutions in 1 country.

Jinjie DuanNHC Key Laboratory of Hormones and Development, Chu Hsien-I Memorial Hospital and Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin, China.ORCID 0009-0001-8809-4456
Wenhui DongNHC Key Laboratory of Hormones and Development, Chu Hsien-I Memorial Hospital and Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin, China.
Guangyan WangNHC Key Laboratory of Hormones and Development, Chu Hsien-I Memorial Hospital and Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin, China.
Wenjing XiuNHC Key Laboratory of Hormones and Development, Chu Hsien-I Memorial Hospital and Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin, China.
Guangyin PuNHC Key Laboratory of Hormones and Development, Chu Hsien-I Memorial Hospital and Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin, China.
Jingwen XuNHC Key Laboratory of Hormones and Development, Chu Hsien-I Memorial Hospital and Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin, China.
Chenji YeHenan Key Laboratory of Medical Tissue Regeneration, Xinxiang Medical University, Xinxiang, China.
Xu ZhangThe Province and Ministry Co-sponsored Collaborative Innovation Center for Medical Epigenetics, Tianjin Medical University, Tianjin, China. xuzhang@tmu.edu.cn.ORCID 0000-0002-8103-8486
Yi ZhuDepartment of Physiology and Pathophysiology, Tianjin Medical University, Tianjin, China. zhuyi@tmu.edu.cn.ORCID 0000-0001-7725-9166
Chunjiong WangNHC Key Laboratory of Hormones and Development, Chu Hsien-I Memorial Hospital and Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin, China. wangchunjiong@tmu.edu.cn.ORCID 0000-0001-7464-267X
Tianjin Medical University · CNXinxiang Medical University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81822006National Natural Science Foundation of China (National Science Foundation of China) 82127808National Natural Science Foundation of China (National Science Foundation of China) 82170635
6 · The paper itself

Abstract

Aging is a major risk factor for metabolic disorders. Polyunsaturated fatty acid-derived bioactive lipids play critical roles as signaling molecules in metabolic processes. Nonetheless, their effects on age-related liver steatosis remain unknown. Here we show that senescent liver cells induce liver steatosis in a paracrine manner. Linoleic acid-derived 9-hydroxy-octadecadienoic acid (9-HODE) and 13-HODE increase in middle-aged (12-month-old) and aged (20-month-old) male mouse livers and conditioned medium from senescent hepatocytes and macrophages. Arachidonate 15-lipoxygenase, an enzyme for 13-HODE and 9-HODE production, is upregulated in senescent cells. A 9-HODE and 13-HODE mixture induces liver steatosis and activates SREBP1. Furthermore, catalase (CAT) is a direct target of 13-HODE, and its activity is decreased by 13-HODE. CAT overexpression reduces 13-HODE-induced liver steatosis and protects male mice against age-related liver steatosis. Therefore, 13-HODE produced by senescent hepatocytes and macrophages activates SREBP1 by directly inhibiting CAT activity and promotes liver steatosis.

Indexed as

Fatty LiverLinoleic AcidsAnimalsCatalaseLinoleic AcidLiverMaleMice13-hydroxy-9,11-octadecadienoic acidCatalaseLinoleic AcidLinoleic Acids

Identifiers

PMID38071367
PMCPMC10710422
OpenAlexW4389504699

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.