Evidence map›Paper›PMID 41716409›Full record

ReviewFrontiers in immunology2026

Renal allograft interstitial fibrosis: multicellular interactions and therapeutic strategies.

Runmin Ding, Qinghuan Shen, Junyi Zhou, Ruoyun Tan, Min Gu, Zijie Wang, Zeping Gui

Abstract readReview
In one paragraph

Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

7 authors.

Runmin Ding *Department of Urology, Jiangsu Key Laboratory of Urological Disease Prevention and Treatment, The Second Affiliated Hospital of Nanjing Medical University, Nanjing Medical University, Nanjing, China.
Qinghuan Shen *Department of Urology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Junyi Zhou *Department of Urology, Jiangsu Key Laboratory of Urological Disease Prevention and Treatment, The Second Affiliated Hospital of Nanjing Medical University, Nanjing Medical University, Nanjing, China.
Ruoyun TanDepartment of Urology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, China.
Min GuDepartment of Urology, Jiangsu Key Laboratory of Urological Disease Prevention and Treatment, The Second Affiliated Hospital of Nanjing Medical University, Nanjing Medical University, Nanjing, China.
Zijie WangDepartment of Urology, Jiangsu Key Laboratory of Urological Disease Prevention and Treatment, The Second Affiliated Hospital of Nanjing Medical University, Nanjing Medical University, Nanjing, China.
Zeping GuiDepartment of Urology, Jiangsu Key Laboratory of Urological Disease Prevention and Treatment, The Second Affiliated Hospital of Nanjing Medical University, Nanjing Medical University, Nanjing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Kidney transplantation remains the most effective treatment for end-stage renal disease (ESRD). However, long-term graft survival is still limited by chronic allograft dysfunction (CAD), which is primarily characterized by renal interstitial fibrosis (RIF). The development of RIF is an actively regulated and progressive process involving both immune and non-immune mechanisms. Within the renal microenvironment, multiple cell populations interact to form a self-reinforcing profibrotic network that ultimately drives irreversible fibrotic remodeling. Despite increasing mechanistic insights, the precise modes of multicellular crosstalk remain incompletely understood, and effective targeted therapies are still lacking in clinical practice. In this review, we systematically summarize the dynamic interactions among immune cells, renal epithelial cells, and stromal cells during renal allograft interstitial fibrosis. By integrating recent advances at the cellular and molecular levels, we identify key regulatory nodes within this multicellular network and discuss emerging therapeutic targets and precision intervention strategies aimed at inhibiting profibrotic signaling, alleviating pathological tissue remodeling, and improving long-term graft function and survival.

Indexed as

AllograftsKidneyKidney TransplantationAnimalsCell CommunicationFibrosisGraft RejectionGraft SurvivalHumansSignal Transductionchronic allograft dysfunction (CAD)immune cellskidney transplantationmulticellular crosstalkrenal allograft interstitial fibrosisrenal cells

Identifiers

PMID41716409
PMCPMC12913155

What Socratic 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 Socratic graph.