Evidence map›Paper›PMID 34116674›Full record

ArticleCardiovascular diabetology2021

Dapagliflozin: a sodium-glucose cotransporter 2 inhibitor, attenuates angiotensin II-induced cardiac fibrotic remodeling by regulating TGFβ1/Smad signaling.

Yuze Zhang, Xiaoyan Lin, Yong Chu, Xiaoming Chen, Heng Du, Hailin Zhang, Changsheng Xu, Hong Xie, Qinyun Ruan, Jinxiu Lin and 4 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cardiovascular diabetology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
9.7field-weighted citation impact, top 1% of its field
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

55 citing papers in PubMed, 95 citations in OpenAlex.

  1. Trial
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  11. SGLT2 inhibition for patients with ADPKD - closing the evidence gap.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2025
    Review
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  18. SGLT2 inhibitors: how do they affect the cardiac cells.Molecular and cellular biochemistry · 2025
    Review
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  20. 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 at 2 institutions in 1 country.

Yuze Zhang *Cardiovascular Department, The First Affiliated Hospital, Fujian Medical University, Fujian Institute of Hypertension, 20 Chazhong Road, Fuzhou, 350005, China.
Xiaoyan Lin *Echocardiological Department, The First Affiliated Hospital, Fujian Medical University, Fuzhou, 350005, China.
Yong ChuCardiovascular Department, The First Affiliated Hospital, Fujian Medical University, Fujian Institute of Hypertension, 20 Chazhong Road, Fuzhou, 350005, China.
Xiaoming ChenEditorial Department of Chinese Journal of Hypertension, Fuzhou, 350005, China.
Heng DuCardiovascular Department, The First Affiliated Hospital, Fujian Medical University, Fujian Institute of Hypertension, 20 Chazhong Road, Fuzhou, 350005, China.
Hailin ZhangCardiovascular Department, The First Affiliated Hospital, Fujian Medical University, Fujian Institute of Hypertension, 20 Chazhong Road, Fuzhou, 350005, China.
Changsheng XuCardiovascular Department, The First Affiliated Hospital, Fujian Medical University, Fujian Institute of Hypertension, 20 Chazhong Road, Fuzhou, 350005, China.
Hong XieCardiovascular Department, The First Affiliated Hospital, Fujian Medical University, Fujian Institute of Hypertension, 20 Chazhong Road, Fuzhou, 350005, China.
Qinyun RuanEchocardiological Department, The First Affiliated Hospital, Fujian Medical University, Fuzhou, 350005, China.
Jinxiu LinCardiovascular Department, The First Affiliated Hospital, Fujian Medical University, Fujian Institute of Hypertension, 20 Chazhong Road, Fuzhou, 350005, China.
Jie LiuSchool of Pharmacy College, Xiamen University, Xiamen, 361102, China.
Jinzhang ZengSchool of Pharmacy College, Xiamen University, Xiamen, 361102, China.
Ke MaClinical Research Center, The First Affiliated Hospital, Fujian Medical University, 20 Chazhong Road, Fuzhou, 350005, China. mke2002@163.com.
Dajun ChaiCardiovascular Department, The First Affiliated Hospital, Fujian Medical University, Fujian Institute of Hypertension, 20 Chazhong Road, Fuzhou, 350005, China. dajunchai@126.com.ORCID 0000-0001-9477-9956
Fujian Medical University · CNXiamen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCardiac remodeling is one of the major risk factors for heart failure. In patients with type 2 diabetes, sodium-glucose cotransporter 2 (SGLT2) inhibitors reduce the risk of the first hospitalization for heart failure, possibly through glucose-independent mechanisms in part, but the underlying mechanisms remain largely unknown. This study aimed to shed light on the efficacy of dapagliflozin in reducing cardiac remodeling and potential mechanisms.

methodsSprague-Dawley (SD) rats, induced by chronic infusion of Angiotensin II (Ang II) at a dose of 520 ng/kg per minute for 4 weeks with ALZET® mini-osmotic pumps, were treated with either SGLT2 inhibitor dapagliflozin (DAPA) or vehicle alone. Echocardiography was performed to determine cardiac structure and function. Cardiac fibroblasts (CFs) were treated with Ang II (1 μM) with or without the indicated concentration (0.5, 1, 10 μM) of DAPA. The protein levels of collagen and TGF-β1/Smad signaling were measured along with body weight, and blood biochemical indexes.

resultsDAPA pretreatment resulted in the amelioration of left ventricular dysfunction in Ang II-infused SD rats without affecting blood glucose and blood pressure. Myocardial hypertrophy, fibrosis and increased collagen synthesis caused by Ang II infusion were significantly inhibited by DAPA pretreatment. In vitro, DAPA inhibit the Ang II-induced collagen production of CFs. Immunoblot with heart tissue homogenates from chronic Ang II-infused rats revealed that DAPA inhibited the activation of TGF-β1/Smads signaling.

conclusionDAPA ameliorates Ang II-induced cardiac remodeling by regulating the TGF-β1/Smad signaling in a non-glucose-lowering dependent manner.

Indexed as

Angiotensin IIAnimalsAntifibrotic AgentsBenzhydryl CompoundsCells, CulturedDisease Models, AnimalFibroblastsFibrosisGlucosidesHypertrophy, Left VentricularMaleMyocardiumRatsRats, Sprague-DawleySignal TransductionSmad ProteinsAngiotensin IIAntifibrotic AgentsBenzhydryl CompoundsdapagliflozinGlucosidesSmad ProteinsSodium-Glucose Transporter 2 InhibitorsTgfb1 protein, ratTransforming Growth Factor beta1Angiotensin IICardiac fibrotic remodelingDapagliflozinSodium–glucose cotransporter 2 inhibitorsTGFβ1/Smad signaling

Identifiers

PMID34116674
PMCPMC8196449
OpenAlexW3137291439

What OpenQuestion holds

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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 OpenQuestion graph.