Evidence map›Paper›PMID 33564685›Full record

ArticleBioMed research international2021

Forskolin Protected against Streptozotocin-Induced Diabetic Cardiomyopathy via Inhibition of Oxidative Stress and Cardiac Fibrosis in Mice.

Xu Zhang, Pei-Xiong Ke, Xun Yuan, Gui-Ping Zhang, Wen-Liang Chen, Gen-Shui Zhang

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Article in BioMed research international, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

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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

9 citing papers in PubMed, 18 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

6 authors at 2 institutions in 2 countries.

Xu ZhangKey Laboratory of Molecular Clinical Pharmacology & Guangzhou Institute of Cardiovascular Disease, Guangzhou Medical University, Guangzhou, Guangdong 511436, China.
Pei-Xiong KeKey Laboratory of Molecular Clinical Pharmacology & Guangzhou Institute of Cardiovascular Disease, Guangzhou Medical University, Guangzhou, Guangdong 511436, China.
Xun YuanKey Laboratory of Molecular Clinical Pharmacology & Guangzhou Institute of Cardiovascular Disease, Guangzhou Medical University, Guangzhou, Guangdong 511436, China.
Gui-Ping ZhangKey Laboratory of Molecular Clinical Pharmacology & Guangzhou Institute of Cardiovascular Disease, Guangzhou Medical University, Guangzhou, Guangdong 511436, China.
Wen-Liang ChenDepartment of Biology, York University, 4700 Keele Street, Toronto, ON, Canada M3J 1P3.ORCID https://orcid.org/0000-0001-5141-325X
Gen-Shui ZhangKey Laboratory of Molecular Clinical Pharmacology & Guangzhou Institute of Cardiovascular Disease, Guangzhou Medical University, Guangzhou, Guangdong 511436, China.ORCID https://orcid.org/0000-0003-0642-1861
Guangzhou Medical University · CNYork University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDiabetic cardiomyopathy is one of the cardiac complications in diabetes patients, eventually resulting in heart failure and increasing morbidity and mortality. Oxidative stress is a critical pathological feature in diabetic hearts, contributing to the development of DCM. Forskolin (FSK) was shown to reduce oxidative stress. This study was aimed at investigating the effects of FSK on diabetic hearts and the relevant molecular mechanisms.

methodsStreptozotocin- (STZ-) induced diabetes in mice was treated with FSK through intraperitoneal injection. Cardiac functions were evaluated by echocardiography. Hematoxylin-eosin and Masson trichrome staining was employed to determine heart morphological changes and cardiac fibrosis, respectively. Cardiac fibrosis-related markers were detected by western blot. Superoxide dismutase activity, reduced/oxidized glutathione ratio, and malondialdehyde concentration in left ventricles were determined using respective commercial kits.

resultsAbnormal cardiac diastolic dysfunction and cardiac fibrosis were observed in diabetic hearts. FSK treatment significantly improved the cardiac diastolic function and attenuated the abnormal morphological change in diabetic hearts. Moreover, FSK treatment in diabetic mice decreased the expression of fibronectin, collagen I, TGF-

conclusionsOur study demonstrates that FSK protects against the development of DCM in STZ-induced diabetes in mice. Our study suggests that FSK might be a potential target for drug development in treating DCM.

Indexed as

ActinsAnimalsApoptosisColforsinDiabetes Mellitus, ExperimentalDiabetic CardiomyopathiesDisease Models, AnimalFibrosisGene Expression RegulationHeartHumansMiceMyocardiumOxidative StressTransforming Growth Factor betaActa2 protein, mouseActinsColforsinTransforming Growth Factor beta

Identifiers

PMID33564685
PMCPMC7867442
OpenAlexW3127685876

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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.