Evidence map›Paper›PMID 39255796›Full record

ArticleCell reports. Medicine2024

Lipolysis engages CD36 to promote ZBP1-mediated necroptosis-impairing lung regeneration in COPD.

Jiazhen Wang, Ru Wang, Yicun Li, Jiahui Huang, Yang Liu, Jiayi Wang, Peng Xian, Yuanhang Zhang, Yanmei Yang, Haojian Zhang and 1 more

Abstract read
In one paragraph

Article in Cell reports. Medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

9 citing papers in PubMed.

  1. Article
  2. Cell death-associated genes as novel diagnostic biomarkers for autism spectrum disorder.Apoptosis : an international journal on programmed cell death · 2026
    Article
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  4. Review
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  6. Article
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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

11 authors.

Jiazhen WangCollaborative Innovation Center for Chinese Medicine and Respiratory Diseases Co-Constructed by Henan Province and Education Ministry of People's Republic of China, Henan University of Chinese Medicine, Zhengzhou, China; Academy of Chinese Medicine Science, Henan University of Chinese Medicine, Zhengzhou, China.
Ru WangCollaborative Innovation Center for Chinese Medicine and Respiratory Diseases Co-Constructed by Henan Province and Education Ministry of People's Republic of China, Henan University of Chinese Medicine, Zhengzhou, China; Academy of Chinese Medicine Science, Henan University of Chinese Medicine, Zhengzhou, China.
Yicun LiPeking University Shenzhen Hospital, Shenzhen Peking University-The Hong Kong University of Science and Technology Medical Center, Shenzhen, China.
Jiahui HuangCollaborative Innovation Center for Chinese Medicine and Respiratory Diseases Co-Constructed by Henan Province and Education Ministry of People's Republic of China, Henan University of Chinese Medicine, Zhengzhou, China; Academy of Chinese Medicine Science, Henan University of Chinese Medicine, Zhengzhou, China.
Yang LiuCollaborative Innovation Center for Chinese Medicine and Respiratory Diseases Co-Constructed by Henan Province and Education Ministry of People's Republic of China, Henan University of Chinese Medicine, Zhengzhou, China.
Jiayi WangCollaborative Innovation Center for Chinese Medicine and Respiratory Diseases Co-Constructed by Henan Province and Education Ministry of People's Republic of China, Henan University of Chinese Medicine, Zhengzhou, China; Academy of Chinese Medicine Science, Henan University of Chinese Medicine, Zhengzhou, China.
Peng XianCollaborative Innovation Center for Chinese Medicine and Respiratory Diseases Co-Constructed by Henan Province and Education Ministry of People's Republic of China, Henan University of Chinese Medicine, Zhengzhou, China; Academy of Chinese Medicine Science, Henan University of Chinese Medicine, Zhengzhou, China.
Yuanhang ZhangCollaborative Innovation Center for Chinese Medicine and Respiratory Diseases Co-Constructed by Henan Province and Education Ministry of People's Republic of China, Henan University of Chinese Medicine, Zhengzhou, China; Academy of Chinese Medicine Science, Henan University of Chinese Medicine, Zhengzhou, China.
Yanmei YangAcademy of Medical Sciences, Zhengzhou University, Zhengzhou, China.
Haojian ZhangFrontier Science Center for Immunology and Metabolism, Wuhan University, Wuhan, China; Taikang Center for Life and Medical Sciences, Wuhan University, Wuhan, China. Electronic address: haojian_zhang@whu.edu.cn.
Jiansheng LiCollaborative Innovation Center for Chinese Medicine and Respiratory Diseases Co-Constructed by Henan Province and Education Ministry of People's Republic of China, Henan University of Chinese Medicine, Zhengzhou, China; Academy of Chinese Medicine Science, Henan University of Chinese Medicine, Zhengzhou, China; Henan Key Laboratory of Chinese Medicine for Respiratory Disease, Henan University of Chinese Medicine, Zhengzhou, China. Electronic address: ljs2015@hactcm.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung parenchyma destruction represents a severe condition commonly found in chronic obstructive pulmonary disease (COPD), a leading cause of morbidity and mortality worldwide. Promoting lung regeneration is crucial for achieving clinical improvement. However, no therapeutic drugs are approved to improve the regeneration capacity due to incomplete understanding of the underlying pathogenic mechanisms. Here, we identify a positive feedback loop formed between adipose triglyceride lipase (ATGL)-mediated lipolysis and overexpression of CD36 specific to lung epithelial cells, contributing to disease progression. Genetic deletion of CD36 in lung epithelial cells and pharmacological inhibition of either ATGL or CD36 effectively reduce COPD pathogenesis and promote lung regeneration in mice. Mechanistically, disruption of the ATGL-CD36 loop rescues Z-DNA binding protein 1 (ZBP1)-induced cell necroptosis and restores WNT/β-catenin signaling. Thus, we uncover a crosstalk between lipolysis and lung epithelial cells, suggesting the regenerative potential for therapeutic intervention by targeting the ATGL-CD36-ZBP1 axis in COPD.

Indexed as

CD36 AntigensLipaseLipolysisLungNecroptosisPulmonary Disease, Chronic ObstructiveRegenerationAcyltransferasesAnimalsEpithelial CellsHumansMaleMiceMice, Inbred C57BLMice, KnockoutRNA-Binding ProteinsAcyltransferasesCD36 AntigensLipasePNPLA2 protein, mouseRNA-Binding ProteinsATGLCD36lipolysislung regenerationnecroptosisZBP1

Identifiers

PMID39255796
PMCPMC11525022

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.