Evidence map›Paper›PMID 26956523›Full record

ArticlePharmacological research2016

Long-term administration of angiotensin (1-7) prevents heart and lung dysfunction in a mouse model of type 2 diabetes (db/db) by reducing oxidative stress, inflammation and pathological remodeling.

Anna M Papinska, Maira Soto, Christopher J Meeks, Kathleen E Rodgers

Open access · greenAbstract read
In one paragraph

Article in Pharmacological research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
8.0field-weighted citation impact, top 3% 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

31 citing papers in PubMed, 55 citations in OpenAlex.

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  17. Diabetic lung disease: fact or fiction?Reviews in endocrine & metabolic disorders · 2019
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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

4 authors at 1 institution in 1 country.

Anna M PapinskaUniversity of Southern California, School of Pharmacy, 1985 Zonal Ave., Los Angeles, CA 90033, USA.
Maira SotoUniversity of Southern California, School of Pharmacy, 1985 Zonal Ave., Los Angeles, CA 90033, USA.
Christopher J MeeksUniversity of Southern California, School of Pharmacy, 1985 Zonal Ave., Los Angeles, CA 90033, USA.
Kathleen E RodgersUniversity of Southern California, School of Pharmacy, 1985 Zonal Ave., Los Angeles, CA 90033, USA. Electronic address: krodgers@usc.edu.
University of Southern California · US

Funding

Angiotensin(1-7): A Target in Diabetic Cardiac IschemiaR01HL082722 · NHLBI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI RODGERS, KATHLEEN E. · 2008 to 2011
$1.4M
Characterizing angiotensin (1-7) to treat immunosuppression in type2 diabetesF31DK103520 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI SOTO, MAIRA · 2015 to 2016
$87k
NHLBI NIH HHS R01 HL082722NIDDK NIH HHS F31 DK103520
6 · The paper itself

Abstract

Congestive heart failure is one of the most prevalent and deadly complications of type 2 diabetes that is frequently associated with pulmonary dysfunction. Among many factors that contribute to development and progression of diabetic complications is angiotensin II (Ang2). Activation of pathological arm of renin-angiotensin system results in increased levels of Ang2 and signaling through angiotensin type 1 receptor. This pathway is well recognized for its role in induction of oxidative stress (OS), inflammation, hypertrophy and fibrosis. Angiotensin (1-7) [A(1-7)], through activation of Mas receptor, opposes the actions of Ang2 which can result in the amelioration of diabetic complications; enhancing the overall welfare of diabetic patients. In this study, 8 week-old db/db mice were administered A(1-7) daily via subcutaneous injections. After 16 weeks of treatment, echocardiographic assessment of heart function demonstrated significant improvement in cardiac output, stroke volume and shortening fraction in diabetic animals. A(1-7) also prevented cardiomyocyte hypertrophy, apoptosis, lipid accumulation, and decreased diabetes-induced fibrosis and OS in the heart tissue. Treatment with A(1-7) reduced levels of circulating proinflammatory cytokines that contribute to the low grade inflammation observed in diabetes. In addition, lung pathologies associated with type 2 diabetes, including fibrosis and congestion, were decreased with treatment. OS and macrophage infiltration were also reduced in the lungs after treatment with A(1-7). Long-term administration of A(1-7) to db/db mice is effective in improving heart and lung function in db/db mice. Treatment prevented pathological remodeling of the tissues and reduced OS, fibrosis and inflammation.

Indexed as

Angiotensin IAnimalsAnti-Inflammatory AgentsAntioxidantsApoptosisCardiotonic AgentsCytokinesDiabetes Mellitus, Type 2Disease Models, AnimalFibrosisHeartHypoglycemic AgentsLipid MetabolismLungMaleMiceAngiotensin Iangiotensin I (1-7)Anti-Inflammatory AgentsAntioxidantsCardiotonic AgentsCytokinesHypoglycemic AgentsPeptide FragmentsAngiotensin (1-7)Diabetes mellitusHeart failureLung congestionRemodeling

Identifiers

PMID26956523
PMCPMC4867244
OpenAlexW2289924150

What OpenQuestion holds

Textmetadata
LicenceTDM
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.