Evidence map›Paper›PMID 38838052›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024

Single-Cell Spatial Transcriptomics Unveils Platelet-Fueled Cycling Macrophages for Kidney Fibrosis.

Jun Liu, Bo Zheng, Qingya Cui, Yu Zhu, Likai Chu, Zhi Geng, Yiming Mao, Lin Wan, Xu Cao, Qianwei Xiong and 5 more

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing 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

25 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Renal IGFBP6 Interacts With THBS1 to Drive Renal Cellular Senescence and Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. MacrophageJournal for immunotherapy of cancer · 2026
    Article
  13. Stem cell therapy targets THBS1 to reverse endometrial fibrosis.Frontiers in cell and developmental biology · 2026
    Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Review
  19. Review
  20. Review
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

15 authors.

Jun LiuPediatric Institute of Soochow University, Children's Hospital of Soochow University, Soochow University, Suzhou, 215025, China.ORCID 0000-0002-0917-7449
Bo ZhengState Key Laboratory of Reproductive Medicine and Offspring Health, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Gusu School of Nanjing Medical University, Suzhou, 215002, China.
Qingya CuiNational Clinical Research Center for Hematologic Diseases, Jiangsu Institute of Hematology, The First Affiliated Hospital of Soochow University, Suzhou, 215006, China.
Yu ZhuPediatric Institute of Soochow University, Children's Hospital of Soochow University, Soochow University, Suzhou, 215025, China.
Likai ChuPediatric Institute of Soochow University, Children's Hospital of Soochow University, Soochow University, Suzhou, 215025, China.
Zhi GengPediatric Institute of Soochow University, Children's Hospital of Soochow University, Soochow University, Suzhou, 215025, China.
Yiming MaoDepartment of Thoracic Surgery, Suzhou Kowloon Hospital, Shanghai Jiao Tong University School of Medicine, Suzhou, 215028, China.
Lin WanPediatric Institute of Soochow University, Children's Hospital of Soochow University, Soochow University, Suzhou, 215025, China.
Xu CaoPediatric Institute of Soochow University, Children's Hospital of Soochow University, Soochow University, Suzhou, 215025, China.
Qianwei XiongPediatric Institute of Soochow University, Children's Hospital of Soochow University, Soochow University, Suzhou, 215025, China.
Fujia GuoDepartment of Microbiology, Immunology & Molecular Genetics, University of California, Los Angeles, CA, 90095, USA.
David C YangDepartment of Internal Medicine, Division of Nephrology, University of California, Davis, CA, 95616, USA.
Ssu-Wei HsuDepartment of Internal Medicine, Division of Nephrology, University of California, Davis, CA, 95616, USA.
Ching-Hsien ChenDepartment of Internal Medicine, Division of Nephrology, University of California, Davis, CA, 95616, USA.
Xiangming YanPediatric Institute of Soochow University, Children's Hospital of Soochow University, Soochow University, Suzhou, 215025, China.

Funding

Gusu Health Talent Project of Suzhou GSWS2020049Gusu Health Talent Project of Suzhou GSWS2022058Key Laboratory Foundation of Structural Deformities in Children of Suzhou SZS2022018National Natural Science Foundation of China 82270713Suzhou Science and Technology Development Plan Project SKY2023002Suzhou Science and Technology Development Plan Project SKY2023059Suzhou Science and Technology Development Plan Project SKY2023194
6 · The paper itself

Abstract

With the increasing incidence of kidney diseases, there is an urgent need to develop therapeutic strategies to combat post-injury fibrosis. Immune cells, including platelets, play a pivotal role in this repair process, primarily through their released cytokines. However, the specific role of platelets in kidney injury and subsequent repair remains underexplored. Here, the detrimental role of platelets in renal recovery following ischemia/reperfusion injury and its contribution to acute kidney injury  to chronic kidney disease transition is aimed to investigated. In this study, it is shown that depleting platelets accelerates injury resolution and significantly reduces fibrosis. Employing advanced single-cell and spatial transcriptomic techniques, macrophages as the primary mediators modulated by platelet signals is identified. A novel subset of macrophages, termed "cycling M2", which exhibit an M2 phenotype combined with enhanced proliferative activity is uncovered. This subset emerges in the injured kidney during the resolution phase and is modulated by platelet-derived thrombospondin 1 (THBS1) signaling, acquiring profibrotic characteristics. Conversely, targeted inhibition of THBS1 markedly downregulates the cycling M2 macrophage, thereby mitigating fibrotic progression. Overall, this findings highlight the adverse role of platelet THBS1-boosted cycling M2 macrophages in renal injury repair and suggest platelet THBS1 as a promising therapeutic target for alleviating inflammation and kidney fibrosis.

Indexed as

Blood PlateletsFibrosisMacrophagesTranscriptomeAcute Kidney InjuryAnimalsDisease Models, AnimalKidneyMaleMiceMice, Inbred C57BLReperfusion InjurySingle-Cell Analysiskidney fibrosismacrophage proliferationplateletthrombospondin 1

Identifiers

PMID38838052
PMCPMC11304276

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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.