Evidence map›Paper›PMID 35413880›Full record

ArticleBMC pulmonary medicine2022

Dapagliflozin, sildenafil and their combination in monocrotaline-induced pulmonary arterial hypertension.

Yi Tang, Siyuan Tan, Minqi Li, Yijin Tang, Xiaoping Xu, Qinghai Zhang, Qinghua Fu, Mingxiang Tang, Jin He, Yi Zhang and 4 more

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

Article in BMC pulmonary medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 4% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

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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 4 institutions in 1 country.

Yi Tang *Department of Cardiology, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Clinical Medicine Research Center of Heart Failure of Hunan Province, Hunan Normal University, Changsha, 410005, China.
Siyuan Tan *Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Changsha, 410005, China.
Minqi LiHunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Changsha, 410005, China.
Yijin TangHunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Changsha, 410005, China.
Xiaoping XuDepartment of Gastroenterology, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Hunan Normal University, Changsha, 410005, China.
Qinghai ZhangDepartment of Cardiology, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Clinical Medicine Research Center of Heart Failure of Hunan Province, Hunan Normal University, Changsha, 410005, China.
Qinghua FuDepartment of Cardiology, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Clinical Medicine Research Center of Heart Failure of Hunan Province, Hunan Normal University, Changsha, 410005, China.
Mingxiang TangDepartment of Cardiology, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Clinical Medicine Research Center of Heart Failure of Hunan Province, Hunan Normal University, Changsha, 410005, China.
Jin HeDepartment of Cardiology, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Clinical Medicine Research Center of Heart Failure of Hunan Province, Hunan Normal University, Changsha, 410005, China.
Yi ZhangDepartment of Cardiology, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Clinical Medicine Research Center of Heart Failure of Hunan Province, Hunan Normal University, Changsha, 410005, China.
Zhaofen ZhengDepartment of Cardiology, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Clinical Medicine Research Center of Heart Failure of Hunan Province, Hunan Normal University, Changsha, 410005, China.
Jianqiang PengDepartment of Cardiology, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Clinical Medicine Research Center of Heart Failure of Hunan Province, Hunan Normal University, Changsha, 410005, China. 2925772400@qq.com.
Tengteng ZhuDepartment of Cardiovascular Medicine, The Second Xiangya Hospital, Central South University, Changsha, 410011, China. zhuxi.teng@163.com.
Wenlin XieDepartment of Pathology, The Seventh Affiliated Hospital of Sun Yat-Sen University, Shenzhen, 518017, China. xiewlin@mail.sysu.edu.cn.
Hunan Provincial People's Hospital · CNHunan Normal University · CNCentral South University · CNThe Seventh Affiliated Hospital of Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDapagliflozin, a selective inhibitor of sodium-glucose cotransporter 2 (SGLT2), can reduce cardiovascular events and mortality in patients with heart failure. A number of mechanisms have been proposed to explain the beneficial effects of SGLT2 inhibitors. The purpose of this study was to determine whether dapagliflozin can improve pulmonary vascular remodelling and the efficacy of dapagliflozin as an add-on therapy to sildenafil in rats with pulmonary arterial hypertension (PAH).

methodsA monocrotaline (MCT)-induced PAH rat model was used in our study. MCT-injected rats were randomly divided into four groups and treated for 3 weeks with daily per os treatment with vehicle, dapagliflozin (1 mg/kg/day), sildenafil (25 mg/kg/day), or a combination of dapagliflozin (1 mg/kg/day) and sildenafil (25 mg/kg/day). Haemodynamic measurements, histological analysis, enzyme-linked immunosorbent assay and western blotting analysis were employed to detect the changes in PAH rats after treatments.

resultsDapagliflozin significantly attenuated MCT-induced increases in right ventricular systolic pressure (RVSP) and right ventricular hypertrophy (RVH) in PAH rats. Dapagliflozin effectively decreased the thickening of pulmonary artery media and decreased the muscularization of pulmonary arterioles in PAH rats. Moreover, dapagliflozin attenuated nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome activation in lung tissues and the levels of interleukin-1β (IL-1β) and interleukin-18 (IL-18) in plasma. However, dapagliflozin as an add-on therapy to sildenafil in rats with PAH did not show a more pronounced beneficial effect on right ventricular systolic pressure and pulmonary vascular remodelling in MCT rats than sildenafil alone.

conclusionsDapagliflozin reduces right ventricular systolic pressure and pulmonary vascular remodelling in a rat model of PAH. However, combination therapy with dapagliflozin and sildenafil was not more effective than monotherapy with sildenafil in PAH rats.

Indexed as

Hypertension, PulmonaryPulmonary Arterial HypertensionAnimalsBenzhydryl CompoundsDisease Models, AnimalFamilial Primary Pulmonary HypertensionGlucosidesHumansMonocrotalinePulmonary ArteryRatsSildenafil CitrateVascular RemodelingBenzhydryl CompoundsdapagliflozinGlucosidesMonocrotalineSildenafil CitrateDapagliflozinPulmonary arterial hypertensionSildenafil

Identifiers

PMID35413880
PMCPMC9006601
OpenAlexW4223542003

What OpenQuestion holds

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LicenceCC BY
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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.