Evidence map›Paper›PMID 42254676›Full record

ArticlePeerJ2026

Dapagliflozin attenuates diabetic renal fibrosis by inhibiting macrophage-myofibroblast transition

Xiaoyun Li, Guoxiang Yao, Honggang Wang, Tingting Zhao, Yujiao Sun, Qi Gao, Zhuo Li, Bing Chen

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PeerJ, 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

8 authors.

Xiaoyun Li *Department of Nephrology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.
Guoxiang Yao *Department of Nephrology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.
Honggang WangDepartment of Nephrology, The Second Qilu Hospital of Shandong University, Jinan, Shandong, China.
Tingting ZhaoDepartment of Respiratory and Critical Care Medicine, Shandong Public Health Clinical Center, Shandong University, Jinan, Shandong, China.
Yujiao SunDepartment of Nephrology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.
Qi GaoDepartment of Nephrology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.
Zhuo LiDepartment of Nephrology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.
Bing ChenDepartment of Nephrology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: Renal fibrosis plays a pivotal role in the progression of renal dysfunction in diabetic kidney disease (DKD), with the macrophage-to-myofibroblast transition (MMT) serving as a central mechanism driving the advancement of renal fibrosis to end-stage renal disease (ESRD) in various chronic kidney conditions. Although the sodium-glucose cotransporter 2 (SGLT2) inhibitor dapagliflozin (DAPA) slows renal function decline in DKD, its antifibrotic mechanisms remain unclear. This study aimed to elucidate whether DAPA ameliorates renal fibrosis by suppressing MMT, and the underlying molecular mechanisms. Methods: We established a DKD model in male C57BL/6J mice by inducing them with a high-fat diet (HFD) followed by streptozotocin (STZ) injection. The effects of DAPA on renal function parameters (serum creatinine (Scr), urinary albumin-to-creatinine ratio (UACR)), and renal pathological injury, fibrosis markers (α-smooth muscle actin (α-SMA), type I collagen (Col-I)) were comprehensively evaluated. Immunofluorescence (IF) and Western blot were employed to analyze MMT progression (F4/80 Results: DAPA significantly reduced blood glucose levels, mitigated weight loss, and effectively inhibited type 2 diabetes-induced increase in Scr (43.78 ± 3.84 Conclusion: This study is the first to reveal that DAPA is highly likely to exert anti-fibrotic effects through a novel mechanism involving targeted modulation of the TGF-β1-Smad3/7 axis to inhibit MMT, thereby laying a theoretical foundation and identifying a potential therapeutic target for precision treatment of DKD.

Indexed as

Benzhydryl CompoundsDiabetic NephropathiesGlucosidesMacrophagesMyofibroblastsSodium-Glucose Transporter 2 InhibitorsAnimalsDiabetes Mellitus, ExperimentalFibrosisKidneyMaleMiceMice, Inbred C57BLSignal TransductionSmad3 ProteinSmad7 ProteinBenzhydryl CompoundsdapagliflozinGlucosidesSmad3 ProteinSmad3 protein, mouseSmad7 ProteinSmad7 protein, mouseSodium-Glucose Transporter 2 InhibitorsTgfb1 protein, mouseTransforming Growth Factor beta1DapagliflozinDiabetic kidney diseaseMacrophage-myofibroblast transition (MMT)Renal fibrosisTGF-β1/Smad

Identifiers

PMID42254676
PMCPMC13242187

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.