Evidence map›Paper›PMID 33495841›Full record

ArticleMolecular medicine reports2021

Allisartan isoproxil attenuates oxidative stress and inflammation through the SIRT1/Nrf2/NF‑κB signalling pathway in diabetic cardiomyopathy rats.

Qinyang Jin, Qin Zhu, Kai Wang, Mengli Chen, Xinli Li

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
6.9field-weighted citation impact, top 2% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.

  1. Pooled it
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  16. Empagliflozin Induces Vascular Relaxation in Rat Coronary Artery Due to Activation of BK Channels.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024
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  17. Potential Mechanisms Underlying the Therapeutic Roles ofCurrent computer-aided drug design · 2024
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  18. Review
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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

5 authors at 3 institutions in 1 country.

Qinyang JinDepartment of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Qin ZhuDepartment of Nephrology, Hangzhou Hospital of Traditional Chinese Medicine, Hangzhou, Zhejiang 310007, P.R. China.
Kai WangDepartment of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Mengli ChenDepartment of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Xinli LiDepartment of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China.
Jiangsu Province Hospital · CNHangzhou Hospital of Traditional Chinese Medicine · CNNanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Allisartan isoproxil is a new nonpeptide angiotensin II receptor blocker (ARB) precursor drug that is used to treat hypertension and reduce the risk of heart disease. The present study explored the effects of allisartan isoproxil on diabetic cardiomyopathy (DCM) and revealed the roles of hyperglycaemia‑induced oxidative stress and inflammation. A rat DCM model was established by high‑fat diet feeding in combination with intraperitoneal injection of streptozocin. Echocardiographs showed that diabetic rats exhibited significantly decreased cardiac function. Troponin T (cTnT) and B‑type natriuretic peptide (BNP) were significantly increased in DCM rats as obtained by ELISA. Allisartan isoproxil significantly improved the EF% and E'/A' ratio. Histopathologic staining showed that allisartan isoproxil prevented histological alterations, attenuated the accumulation of collagen, and ameliorated cTnT and BNP levels. Western blot and immunohistochemical results indicated that the expression levels of silent information regulator 2 homologue 1 (SIRT1) and nuclear factor erythroid 2‑related factor 2 (Nrf2) were decreased in the hearts of diabetic rats, and antioxidant defences were also decreased. In addition, allisartan isoproxil decreased the expression of NF‑κB p65 and the inflammatory cytokines TNF‑α and IL‑1β which were determined by reverse transcription‑quantitative PCR in the diabetic heart. Western blotting and TUNEL staining results also showed that cardiac Bax and cleaved caspase‑3 and the number of apoptotic myocardial cells were increased in the diabetic heart and decreased following treatment with allisartan isoproxil. In conclusion, the present results indicated that allisartan isoproxil alleviated DCM by attenuating diabetes‑induced oxidative stress and inflammation through the SIRT1/Nrf2/NF‑κB signalling pathway.

Indexed as

AnimalsBiphenyl CompoundsDiabetes Mellitus, ExperimentalDiabetic CardiomyopathiesImidazolesInflammationNF-E2-Related Factor 2NF-kappa BOxidative StressRatsRats, Sprague-DawleySignal TransductionSirtuin 1allisartan isoproxilBiphenyl CompoundsImidazolesNfe2l2 protein, ratNF-E2-Related Factor 2NF-kappa BSirt1 protein, ratSirtuin 1allisartan isoproxildiabetic cardiomyopathyinflammationNF‑κBnuclear factor erythroid 2‑related factor 2oxidative stresssilent information regulator 2 homologue 1

Identifiers

PMID33495841
PMCPMC7845586
OpenAlexW3124098430

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.