Evidence map›Paper›PMID 34324657›Full record

ArticleCardiovascular research2022

Resistin deletion protects against heart failure injury by targeting DNA damage response.

Baoyin Zhao, Rihab Bouchareb, Djamel Lebeche

Open access · bronzeAbstract read
In one paragraph

Article in Cardiovascular research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.1field-weighted citation impact, top 7% 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

24 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. DNA damage and repair in cardiomyopathy: mechanisms and therapeutic opportunities.American journal of physiology. Heart and circulatory physiology · 2026
    Review
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  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
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  13. Review
  14. Article
  15. Review
  16. Adipokines and Their Role in Heart Failure: A Literature Review.The Journal of innovations in cardiac rhythm management · 2023
    Review
  17. Review
  18. Article
  19. Article
  20. Review
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

3 authors at 1 institution in 1 country.

Baoyin ZhaoCardiovascular Research Institute, New York, NY 10029, USA.
Rihab BoucharebCardiovascular Research Institute, New York, NY 10029, USA.
Djamel LebecheCardiovascular Research Institute, New York, NY 10029, USA.ORCID 0000-0002-7911-2923
Cardiovascular Research Foundation · US

Funding

TRAINING PROGRAM IN MOLECULAR AND CELLULAR CARDIOLOGYT32HL007824 · NHLBI · MOUNT SINAI SCHOOL OF MEDICINE OF NYU · PI GELB, BRUCE D · 1995 to 2022
$8.6M
Genetic Analysis of microRNAs Function in Diabetic CardiomyopathyR01HL097357 · NHLBI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI LEBECHE, DJAMEL · 2010 to 2014
$2.1M
Molecular and Metabolic phenotype of Impaired AdipoR1 in the HeartR01HL137220 · NHLBI · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI LEBECHE, DJAMEL · 2017 to 2020
$1.7M
NHLBI NIH HHS R01 HL097357NHLBI NIH HHS R01 HL137220NHLBI NIH HHS T32 HL007824
6 · The paper itself

Abstract

aimsIncreased resistin (Retn) levels are associated with development of cardiovascular diseases. However, the role of Retn in heart failure (HF) is still unclear. Here we probed the functional and molecular mechanism underlying the beneficial effect of Retn deletion in HF. METHODS AND

resultsWild-type (WT) and adipose tissue-specific Retn-knockout (RKO) mice were subjected to transverse aortic constriction (TAC)-induced HF. Cardiac function and haemodynamic changes were measured by echocardiography and left ventricular catheterization. Adipose tissue Retn deletion attenuated while Retn cardiac-selective overexpression, via a recombinant adeno-associated virus-9 vector, exacerbated TAC-induced hypertrophy, cardiac dysfunction, and myocardial fibrosis in WT and RKO mice. Mechanistically, we showed that Gadd45α was significantly increased in RKO HF mice while cardiac overexpression of Retn led to its downregulation. miR148b-3p directly targets Gadd45α and inhibits its expression. Retn overexpression upregulated miR148b-3p expression and triggered DNA damage response (DDR) in RKO-HF mice. Inhibition of miR148b-3p in vivo normalized Gadd45α expression, decreased DDR, and reversed cardiac dysfunction and fibrosis. In vitro Retn overexpression in adult mouse cardiomyocytes activated miR148b-3p and reduced Gadd45α expression. Gadd45α overexpression in H9C2-cardiomyoblasts protected against hydrogen peroxide- and Retn-induced DDR.

conclusionThese findings reveal that diminution in circulating Retn reduced myocardial fibrosis and apoptosis, and improved heart function in a mouse model of HF, at least in part, through attenuation of miR148b-3p and DDR. The results of this study indicate that controlling Retn levels may provide a potential therapeutic approach for treating pressure overload-induced HF.

Indexed as

DNA DamageHeart FailureResistinAnimalsDisease Models, AnimalFibrosisMiceMice, Inbred C57BLMice, KnockoutMyocytes, CardiacVentricular RemodelingResistinRetn protein, mouseDNA damage responseGadd45αmiR148b-3pPressure overload heart failureResistin

Identifiers

PMID34324657
PMCPMC9239578
OpenAlexW3184162537

What OpenQuestion holds

Textmetadata
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.