Evidence map›Paper›PMID 42807847›Full record

ArticleInternational journal of biological sciences2026

Tubular NAT10 Promotes the Secretion of TGF-β and Lactate to Drive Fibroblast Activation in Diabetic Kidney Disease.

Jinfang Lu, Yuqing Feng, Xujun Peng, Zijin He, Zhou Li, Ao Jia, Yaohui Bao, Lingui Xie, Renchun Wang, Wenbo Zhang and 6 more

Abstract read
PubMed Full text at PMC Publisher
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
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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

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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

16 authors.

Jinfang LuDepartment of Critical Care Medicine, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.
Yuqing FengDepartment of Ophthalmology, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.
Xujun PengDepartment of Ophthalmology, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.
Zijin HeDepartment of Ophthalmology, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.
Zhou LiDepartment of Ophthalmology, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.
Ao JiaDepartment of Ophthalmology, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.
Yaohui BaoDepartment of Ophthalmology, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.
Lingui XieDepartment of Ophthalmology, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.
Renchun WangDepartment of Ophthalmology, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.
Wenbo ZhangDepartment of Critical Care Medicine, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.
Qin KangDepartment of Critical Care Medicine, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.
Yanyan ZhouDepartment of Critical Care Medicine, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.
Cheng WangDivision of Nephrology, Department of Medicine, the Fifth Affiliated Hospital of Sun Yat-Sen University, Zhuhai, Guangdong 519000, China.
Hongquan PengDepartment of Nephrology, Kiang Wu Hospital, Macau SAR 999078, China.
Huiling LiDepartment of Ophthalmology, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.
Dongshan ZhangDepartment of Critical Care Medicine, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In advanced diabetic kidney disease (DKD), tubulointerstitial fibrosis (TIF) is a key histopathological lesion accompanying progressive renal functional decline. However, the tubular mechanisms that drive tubulointerstitial fibrogenesis remain incompletely understood. N-acetyltransferase 10 (NAT10) mediates mRNA N4-acetylcytidine (ac4C) modification, but its role and therapeutic potential in DKD are unknown. We investigated NAT10 regulation and function using cultured tubular cells, diabetic mouse models, patient kidney specimens, and tubule-specific Nat10 knockout mice, together with pharmacological treatment using guanosine diphosphate disodium salt. High glucose or diabetes increased tubular NAT10 abundance in cultured cells, mouse kidneys, and human DKD tissues through activation of NF-κB signaling. Mechanistically, NAT10 in tubular cells stabilized

Indexed as

Diabetic NephropathiesFibroblastsKidney TubulesTransforming Growth Factor betaAnimalsBromodomain Containing ProteinsHumansMaleMiceMice, Inbred C57BLMice, KnockoutSignal TransductionTranscription FactorsBromodomain Containing ProteinsTranscription FactorsTransforming Growth Factor betaac4C modificationdiabetic kidney diseaselactateNAT10TGF-β signalingtubulointerstitial fibrosis

Identifiers

PMID42807847
PMCPMC13617997

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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.