Evidence map›Paper›PMID 40451900›Full record

ArticleFunctional & integrative genomics2025

Functional genomics reveals adipose-kidney crosstalk as a contributor to kidney fibrosis via the OSM-OSMR pathway.

Jing Zhang, Zhaojun Liu, Shihui Dong, Kun Xu, Kangchun Wang, Luyu Gong, Qiaoqiao Liu, Yue Guo, Yeping Zhu, Jingrong She and 4 more

Abstract read
PubMed Publisher
In one paragraph

Article in Functional & integrative genomics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. Exosome-basedRegenerative biomaterials · 2025
    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.

Jing ZhangNational Clinical Research Center for Kidney Diseases, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, 210093, Jiangsu, China.
Zhaojun LiuJiangsu Key Laboratory of Molecular Medicine, Medical School, Nanjing University, Nanjing, 210093, Jiangsu, China.
Shihui DongNational Clinical Research Center for Kidney Diseases, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, 210093, Jiangsu, China.
Kun XuNational Clinical Research Center for Kidney Diseases, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, 210093, Jiangsu, China.
Kangchun WangNational Clinical Research Center for Kidney Diseases, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, 210093, Jiangsu, China.
Luyu GongJiangsu Key Laboratory of Molecular Medicine, Medical School, Nanjing University, Nanjing, 210093, Jiangsu, China.
Qiaoqiao LiuNational Clinical Research Center for Kidney Diseases, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, 210093, Jiangsu, China.
Yue GuoJiangsu Key Laboratory of Molecular Medicine, Medical School, Nanjing University, Nanjing, 210093, Jiangsu, China.
Yeping ZhuJiangsu Key Laboratory of Molecular Medicine, Medical School, Nanjing University, Nanjing, 210093, Jiangsu, China.
Jingrong SheNational Clinical Research Center for Kidney Diseases, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, 210093, Jiangsu, China.
Song JiangNational Clinical Research Center for Kidney Diseases, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, 210093, Jiangsu, China.
Shaolin ShiNational Clinical Research Center for Kidney Diseases, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, 210093, Jiangsu, China. shaolin.shi@nju.edu.cn.
Zhihong LiuNational Clinical Research Center for Kidney Diseases, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, 210093, Jiangsu, China. liuzhihong@nju.edu.cn.
Jingping YangNational Clinical Research Center for Kidney Diseases, Jinling Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, 210093, Jiangsu, China. jpyang@nju.edu.cn.

Funding

National Key Research and Development Program of China 2024YFC2511002
6 · The paper itself

Abstract

Kidney injury is a severe complication of type 2 diabetes, yet its pathophysiology varies among patients. Although abnormal adipose has been identified as an indicator for the risk of kidney injury in type 2 diabetes, the underlying mechanisms remain unclear. Here, we integrated adipose functional genomics and genome-wide association studies of diabetic nephropathy (DN) to investigate the relationship between adipose and kidney injury. By generating the epigenome, transcriptome and regulatome, we constructed functional genomics map of adipose, revealing the regulatory role of perirenal adipose tissue in kidney disease. Integration of the functional genomics with genetic risk demonstrated that the genetic risk of DN is mediated not only through the kidney itself but also via adipose-kidney crosstalk. Our results revealed that risk variant rs2412980 functions through an adipose-specific regulatory element to control the expression of OSM, encoding the cytokine oncostatin-M. Adipose-derived OSM can reprogram OSMR-expressing renal fibroblasts, and subsequent activation of OSM-OSMR pathway is associated with advanced kidney injury, including reduced eGFR, elevated proteinuria and creatinine levels. Our work confirmed the linkage between adipose and kidney diseases with the genetic evidence, and revealed that the adipo-renal axis promotes the fibrosis of kidney under diabetes through the OSM-OSMR pathway.

Indexed as

Adipose TissueDiabetes Mellitus, Type 2Diabetic NephropathiesKidneyAnimalsFibrosisGenome-Wide Association StudyGenomicsHumansMaleMiceSignal TransductionDiabetic nephropathyFunctional genomicsGenetic riskOSM-OSMR pathwayPerirenal adipose tissueTranscriptional regulation

Identifiers

PMID40451900

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.