Evidence map›Paper›PMID 40330661›Full record

ArticleResearch (Washington, D.C.)2025

Single-Cell RNA Sequencing Analysis Reveals the Role of Macrophage-Mediated CD44-AKT-CCL2 Pathways in Renal Tubule Injury during Calcium Oxalate Crystal Formation.

Xi Jin, Zhongyu Jian, Yucheng Ma, Jun Wen, Ningning Chao, Xiaoting Chen, Liyuan Xiang, Yiqiong Yuan, Linhu Liu, Ya Li and 4 more

Abstract read
In one paragraph

Article in Research (Washington, D.C.), 2025. 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. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. M2 Macrophages Attenuate AQP2Research (Washington, D.C.) · 2026
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  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

14 authors.

Xi JinDepartment of Urology, Institute of Urology (Laboratory of Reconstructive Urology), West China Hospital, Sichuan University, Chengdu, Sichuan, P.R. China.
Zhongyu JianDepartment of Urology, Institute of Urology (Laboratory of Reconstructive Urology), West China Hospital, Sichuan University, Chengdu, Sichuan, P.R. China.
Yucheng MaDepartment of Urology, Institute of Urology (Laboratory of Reconstructive Urology), West China Hospital, Sichuan University, Chengdu, Sichuan, P.R. China.
Jun WenDepartment of Urology, Institute of Urology (Laboratory of Reconstructive Urology), West China Hospital, Sichuan University, Chengdu, Sichuan, P.R. China.
Ningning ChaoDepartment of Pulmonary and Critical Care Medicine, Institute of Respiratory Health, State Key Laboratory of Respiratory Health and Multimorbidity, Frontiers Science Center for Disease-related Molecular Network, Sichuan Provincial Engineering Laboratory of Precision Medicine, Precision Medicine Key Laboratory of Sichuan Province, West China Hospital, West China School of Medicine, Sichuan University, Chengdu 610041, Sichuan Province, P.R. China.
Xiaoting ChenAnimal Experimental Center, West China Hospital, Sichuan University, Chengdu, Sichuan, P.R. China.
Liyuan XiangDepartment of Urology, Institute of Urology (Laboratory of Reconstructive Urology), West China Hospital, Sichuan University, Chengdu, Sichuan, P.R. China.
Yiqiong YuanDepartment of Urology, Institute of Urology (Laboratory of Reconstructive Urology), West China Hospital, Sichuan University, Chengdu, Sichuan, P.R. China.
Linhu LiuDepartment of Urology, Institute of Urology (Laboratory of Reconstructive Urology), West China Hospital, Sichuan University, Chengdu, Sichuan, P.R. China.
Ya LiDepartment of Urology, Institute of Urology (Laboratory of Reconstructive Urology), West China Hospital, Sichuan University, Chengdu, Sichuan, P.R. China.
Jingwen WeiDepartment of Urology, Institute of Urology (Laboratory of Reconstructive Urology), West China Hospital, Sichuan University, Chengdu, Sichuan, P.R. China.
Banghua LiaoDepartment of Urology, Institute of Urology (Laboratory of Reconstructive Urology), West China Hospital, Sichuan University, Chengdu, Sichuan, P.R. China.
Li ZhangDepartment of Pulmonary and Critical Care Medicine, Institute of Respiratory Health, State Key Laboratory of Respiratory Health and Multimorbidity, Frontiers Science Center for Disease-related Molecular Network, Sichuan Provincial Engineering Laboratory of Precision Medicine, Precision Medicine Key Laboratory of Sichuan Province, West China Hospital, West China School of Medicine, Sichuan University, Chengdu 610041, Sichuan Province, P.R. China.
Kunjie WangDepartment of Urology, Institute of Urology (Laboratory of Reconstructive Urology), West China Hospital, Sichuan University, Chengdu, Sichuan, P.R. China.ORCID https://orcid.org/0000-0001-8289-2791

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxalate-induced crystalline kidney injury is a common form of crystal nephropathy. The accumulation of calcium oxalate (CaOx) crystal could lead to renal epithelium injury and inflammation. The underlying cellular events in kidney after CaOx crystal formation are largely unknown. This study was aimed to gain a better understanding of mouse kidney function in the development of renal CaOx formation. The study utilized a mouse CaOx model to analyze the cellular response at 5 time points using single-cell RNA sequencing and investigate the interaction of different cells during renal CaOx crystal formation. Additionally, the study investigated the communication between these cells and macrophages, as well as the role of chemokines in recruiting infiltrating macrophages. RNA velocity analysis uncovered an alternative differentiation pathway for injured and S1 proximal tubule cells, which mainly communicate with macrophages through the SPP1-CD44 pair, along with the expression of proinflammatory factors and stone matrix genes during renal CaOx crystal formation. Furthermore, resident Fn1 macrophages were found to express chemokines, such as CCL2, which recruited infiltrating macrophages. The CCL2 secretion was mediated by the CD44-AKT pathway. Blocking CCL2 decreased the expression of injury markers in the kidney, including CLU, LCN2, and KIM-1, and inhibited CaOx crystal deposition. The study identified potential cell types and target genes involved in renal tubule injury in oxalate-related crystal nephropathy. The findings shed light on the cellular processes that contribute to the formation and damage caused by CaOx crystals within the kidney, which could lead to the development of potential cell types and target genes for treating this condition.

Identifiers

PMID40330661
PMCPMC12053376

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.