Evidence map›Paper›PMID 42328432›Full record

ArticleInternational journal of biological sciences2026

Fibrillin-1 Orchestrates a Pro-senescent Niche Driving Peritubular Endothelial Senescence via ZEB1/endothelin-1/β-catenin Signaling.

Junxin Huang, Xiaoyao Zhang, Zifu Yao, Yuxi Zhang, Di Huang, Yongsi Liu, Fan Fan Hou, Youhua Liu, Li Li

Abstract read
In one paragraph

Article in International journal of biological sciences, 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

9 authors.

Junxin HuangState Key Laboratory of Multi-organ Injury Prevention and Treatment, National Clinical Research Center for Kidney and Urological Diseases, Division of Nephrology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Xiaoyao ZhangState Key Laboratory of Multi-organ Injury Prevention and Treatment, National Clinical Research Center for Kidney and Urological Diseases, Division of Nephrology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Zifu YaoState Key Laboratory of Multi-organ Injury Prevention and Treatment, National Clinical Research Center for Kidney and Urological Diseases, Division of Nephrology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Yuxi ZhangState Key Laboratory of Multi-organ Injury Prevention and Treatment, National Clinical Research Center for Kidney and Urological Diseases, Division of Nephrology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Di HuangLight Innovation Technology Ltd., Shenzhen, China.
Yongsi LiuLight Innovation Technology Ltd., Shenzhen, China.
Fan Fan HouState Key Laboratory of Multi-organ Injury Prevention and Treatment, National Clinical Research Center for Kidney and Urological Diseases, Division of Nephrology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Youhua LiuState Key Laboratory of Multi-organ Injury Prevention and Treatment, National Clinical Research Center for Kidney and Urological Diseases, Division of Nephrology, Nanfang Hospital, Southern Medical University, Guangzhou, China.
Li LiState Key Laboratory of Multi-organ Injury Prevention and Treatment, National Clinical Research Center for Kidney and Urological Diseases, Division of Nephrology, Nanfang Hospital, Southern Medical University, Guangzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Microvascular rarefaction is a predominant pathological hallmark of chronic kidney disease (CKD), functioning simultaneously as a catalyst and consequence of progressive renal compromise. Although endothelial senescence constitutes a cardinal mediator of microvascular attrition in CKD, its upstream regulatory mechanism remains elusive. Here, using integrated single-cell/spatial transcriptomics, decellularized scaffold modeling, diverse murine CKD models, vascular ultrasonography, and tissue-clearing-enabled 3D imaging, we identify fibrillin-1 (FBN1), a core constituent of the fibrogenic niche, as an architect of a pro-senescent microenvironment that directly triggers endothelial senescence. Mechanistically, FBN1 upregulates the transcription factor ZEB1, which binds to the

Indexed as

beta CateninEndothelin-1Fibrillin-1Zinc Finger E-box-Binding Homeobox 1AdipokinesAnimalsCellular SenescenceEndothelial CellsHumansMiceRenal Insufficiency, ChronicSignal TransductionAdipokinesbeta CateninEndothelin-1Fbn1 protein, mouseFibrillin-1ZEB1 protein, mouseZinc Finger E-box-Binding Homeobox 1chronic kidney diseaseendothelial senescencefibrillin-1microvascular rarefactionpro-senescent niche

Identifiers

PMID42328432
PMCPMC13282740

What OpenQuestion holds

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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.