Evidence map›Paper›PMID 38570797›Full record

ReviewLipids in health and disease2024

The novel molecular mechanism of pulmonary fibrosis: insight into lipid metabolism from reanalysis of single-cell RNA-seq databases.

Xiangguang Shi, Yahui Chen, Mengkun Shi, Fei Gao, Lihao Huang, Wei Wang, Dong Wei, Chenyi Shi, Yuexin Yu, Xueyi Xia and 6 more

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Lipids in health and disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
12.1field-weighted citation impact, top 1% 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

26 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
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  16. Altered Metabolism in Idiopathic Pulmonary Fibrosis.Journal of cellular physiology · 2025
    Review
  17. Observational
  18. Article
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  20. Observational
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

16 authors at 7 institutions in 2 countries.

Xiangguang Shi *Department of Dermatology, Huashan Hospital, and State Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, China.
Yahui Chen *Human Phenome Institute, and Collaborative Innovation Center for Genetics and Development, Fudan University, Shanghai, China Fudan University, Shanghai, China.
Mengkun Shi *Department of Thoracic Surgery, Huashan Hospital, Fudan University, Shanghai, China.
Fei Gao *Wuxi Lung Transplant Center, Wuxi People's Hospital affiliated to Nanjing Medical University, Wuxi, China.
Lihao HuangShanghai Key Laboratory of Metabolic Remodeling and Health, Institute of Metabolism & Integrative Biology, Liver Cancer Institute, Zhongshan Hospital, Fudan University, Shanghai, 200438, China.
Wei WangWuxi Lung Transplant Center, Wuxi People's Hospital affiliated to Nanjing Medical University, Wuxi, China.
Dong WeiWuxi Lung Transplant Center, Wuxi People's Hospital affiliated to Nanjing Medical University, Wuxi, China.
Chenyi ShiMOE Key Laboratory of Contemporary Anthropology, School of Life Sciences, Fudan University, Shanghai, China.
Yuexin YuHuman Phenome Institute, and Collaborative Innovation Center for Genetics and Development, Fudan University, Shanghai, China Fudan University, Shanghai, China.
Xueyi XiaHuman Phenome Institute, and Collaborative Innovation Center for Genetics and Development, Fudan University, Shanghai, China Fudan University, Shanghai, China.
Nana SongDepartment of Nephrology, Zhongshan Hospital, Fudan University, Fudan Zhangjiang Institute, Shanghai, People's Republic of China.
Xiaofeng ChenDepartment of Thoracic Surgery, Huashan Hospital, Fudan University, Shanghai, China.
Jörg H W DistlerDepartment of Internal Medicine 3 and Institute for Clinical Immunology, University of Erlangen, Nuremberg, Germany.
Chenqi LuMOE Key Laboratory of Contemporary Anthropology, School of Life Sciences, Fudan University, Shanghai, China. luchenqi@fudan.edu.cn.
Jingyu ChenWuxi Lung Transplant Center, Wuxi People's Hospital affiliated to Nanjing Medical University, Wuxi, China. chenjy@wuxiph.com.
Jiucun WangDepartment of Dermatology, Huashan Hospital, and State Key Laboratory of Genetic Engineering, School of Life Sciences, Fudan University, Shanghai, China. jcwang@fudan.edu.cn.
Fudan University · CNNanjing Medical University · CNHuashan Hospital · CNZhongshan Hospital · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNFriedrich-Alexander-Universität Erlangen-Nürnberg · DEWuxi People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary fibrosis (PF) is a severe pulmonary disease with limited available therapeutic choices. Recent evidence increasingly points to abnormal lipid metabolism as a critical factor in PF pathogenesis. Our latest research identifies the dysregulation of low-density lipoprotein (LDL) is a new risk factor for PF, contributing to alveolar epithelial and endothelial cell damage, and fibroblast activation. In this study, we first integrative summarize the published literature about lipid metabolite changes found in PF, including phospholipids, glycolipids, steroids, fatty acids, triglycerides, and lipoproteins. We then reanalyze two single-cell RNA-sequencing (scRNA-seq) datasets of PF, and the corresponding lipid metabolomic genes responsible for these lipids' biosynthesis, catabolism, transport, and modification processes are uncovered. Intriguingly, we found that macrophage is the most active cell type in lipid metabolism, with almost all lipid metabolic genes being altered in macrophages of PF. In type 2 alveolar epithelial cells, lipid metabolic differentially expressed genes (DEGs) are primarily associated with the cytidine diphosphate diacylglycerol pathway, cholesterol metabolism, and triglyceride synthesis. Endothelial cells are partly responsible for sphingomyelin, phosphatidylcholine, and phosphatidylethanolamines reprogramming as their metabolic genes are dysregulated in PF. Fibroblasts may contribute to abnormal cholesterol, phosphatidylcholine, and phosphatidylethanolamine metabolism in PF. Therefore, the reprogrammed lipid profiles in PF may be attributed to the aberrant expression of lipid metabolic genes in different cell types. Taken together, these insights underscore the potential of targeting lipid metabolism in developing innovative therapeutic strategies, potentially leading to extended overall survival in individuals affected by PF.

Indexed as

Pulmonary FibrosisCholesterolEndothelial CellsHumansLipid MetabolismPhosphatidylcholinesPhospholipidsSingle-Cell Gene Expression AnalysisCholesterolPhosphatidylcholinesPhospholipidsLipid metabolismLipid metabolomic gene, Single-cell RNA-sequencing reanalysisPulmonary fibrosis

Identifiers

PMID38570797
PMCPMC10988923
OpenAlexW4393856099

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.