Evidence map›Paper›PMID 39160276›Full record

ArticleThe EMBO journal2024

PCPE-1, a brown adipose tissue-derived cytokine, promotes obesity-induced liver fibrosis.

Yung Ting Hsiao, Yohko Yoshida, Shujiro Okuda, Manabu Abe, Seiya Mizuno, Satoru Takahashi, Hironori Nakagami, Ryuichi Morishita, Kenya Kamimura, Shuji Terai and 8 more

Abstract read
In one paragraph

Article in The EMBO journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. Multicellular senescence programs in the aged heart.Journal of molecular and cellular cardiology plus · 2026
    Review
  5. PCPE1 and PCPE2: When Sequence Similarity Masks Functional Diversity.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. 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

18 authors.

Yung Ting HsiaoDepartment of Cardiovascular Aging, National Cerebral and Cardiovascular Center Research Institute, Osaka, 564-8565, Japan.
Yohko YoshidaDepartment of Cardiovascular Biology and Medicine, Juntendo University Graduate School of Medicine, Tokyo, 113-8421, Japan.
Shujiro OkudaDivision of Bioinformatics, Niigata University Graduate School of Medical and Dental Sciences, Niigata, 951-8510, Japan.
Manabu AbeDepartment of Cellular Neurobiology, Brain Research Institute, Niigata University, Niigata, 951-8585, Japan.ORCID http://orcid.org/0000-0001-8534-2138
Seiya MizunoLaboratory Animal Resource Center in Transborder Medical Research Center, Institute of Medicine, University of Tsukuba, Ibaraki, 305-8577, Japan.ORCID http://orcid.org/0000-0002-6740-5817
Satoru TakahashiLaboratory Animal Resource Center in Transborder Medical Research Center, Institute of Medicine, University of Tsukuba, Ibaraki, 305-8577, Japan.ORCID http://orcid.org/0000-0002-8540-7760
Hironori NakagamiDepartment of Health Development and Medicine, Osaka University Graduate School of Medicine, Osaka, 565-0871, Japan.ORCID http://orcid.org/0000-0003-4494-3601
Ryuichi MorishitaDepartment of Health Development and Medicine, Osaka University Graduate School of Medicine, Osaka, 565-0871, Japan.
Kenya KamimuraDivision of Gastroenterology and Hepatology, Graduate School of Medical and Dental Sciences, Niigata University, Niigata, 951-8510, Japan.ORCID http://orcid.org/0000-0001-7182-4400
Shuji TeraiDivision of Gastroenterology and Hepatology, Graduate School of Medical and Dental Sciences, Niigata University, Niigata, 951-8510, Japan.ORCID http://orcid.org/0000-0002-5439-635X
Tin May AungDepartment of Cardiovascular Aging, National Cerebral and Cardiovascular Center Research Institute, Osaka, 564-8565, Japan.ORCID http://orcid.org/0000-0001-6873-9643
Ji LiDepartment of Cardiology, 2nd Affiliated Hospital of Harbin Medical University, Harbin, 150001, PR China.
Takaaki FurihataDepartment of Cardiovascular Biology and Medicine, Juntendo University Graduate School of Medicine, Tokyo, 113-8421, Japan.
Jing Yuan TangDepartment of Cardiovascular Biology and Medicine, Juntendo University Graduate School of Medicine, Tokyo, 113-8421, Japan.
Kenneth WalshDivision of Cardiovascular Medicine, Robert M. Berne Cardiovascular Research Center, University of Virginia School of Medicine, Charlottesville, VA, 22908, USA.
Akihito IshigamiMolecular Regulation of Aging, Tokyo Metropolitan Institute for Geriatrics and Gerontology, Tokyo, 173-0015, Japan.ORCID http://orcid.org/0000-0001-7875-7482
Tohru MinaminoDepartment of Cardiovascular Biology and Medicine, Juntendo University Graduate School of Medicine, Tokyo, 113-8421, Japan.ORCID http://orcid.org/0000-0003-1627-6151
Ippei ShimizuDepartment of Cardiovascular Aging, National Cerebral and Cardiovascular Center Research Institute, Osaka, 564-8565, Japan. shimizu.ippei@ncvc.go.jp.ORCID http://orcid.org/0000-0003-3333-8131

Funding

Japan Agency for Medical Research and Development (AMED) JP21gm5010002MEXT | Japan Science and Technology Agency (JST) JPMJFR200LMEXT | Japan Society for the Promotion of Science (JSPS) 16H06244MEXT | Japan Society for the Promotion of Science (JSPS) 17K19648MEXT | Japan Society for the Promotion of Science (JSPS) 22K08215MEXT | Japan Society for the Promotion of Science (JSPS) 23K19579MEXT | Japan Society for the Promotion of Science (JSPS) 23K27602MEXT | Japan Society for the Promotion of Science (JSPS) 24K18656
6 · The paper itself

Abstract

Metabolic dysfunction-associated steatohepatitis (MASH, previously termed non-alcoholic steatohepatitis (NASH)), is a major complication of obesity that promotes fatty liver disease. MASH is characterized by progressive tissue fibrosis and sterile liver inflammation that can lead to liver cirrhosis, cancer, and death. The molecular mechanisms of fibrosis in MASH and its systemic control remain poorly understood. Here, we identified the secreted-type pro-fibrotic protein, procollagen C-endopeptidase enhancer-1 (PCPE-1), as a brown adipose tissue (BAT)-derived adipokine that promotes liver fibrosis in a murine obesity-induced MASH model. BAT-specific or systemic PCPE-1 depletion in mice ameliorated liver fibrosis, whereas, PCPE-1 gain of function in BAT enhanced hepatic fibrosis. High-calorie diet-induced ER stress increased PCPE-1 production in BAT through the activation of IRE-1/JNK/c-Fos/c-Jun signaling. Circulating PCPE-1 levels are increased in the plasma of MASH patients, suggesting a therapeutic possibility. In sum, our results uncover PCPE-1 as a novel systemic control factor of liver fibrosis.

Indexed as

Adipose Tissue, BrownLiver CirrhosisObesityAnimalsCytokinesDisease Models, AnimalEndoplasmic Reticulum StressHumansMaleMiceMice, Inbred C57BLNon-alcoholic Fatty Liver DiseaseSignal TransductionCytokinesBATokineFibrosisMASHObesityPCPE-1

Identifiers

PMID39160276
PMCPMC11535236

What Socratic holds

Textmetadata
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 Socratic graph.