Evidence map›Paper›PMID 25879081›Full record

ArticleJournal of nature and science2015

Harnessing fetal and adult genetic reprograming for therapy of heart disease.

Shyam Sundar Nandi, Paras Kumar Mishra

Abstract read
In one paragraph

Article in Journal of nature and science, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–field-weighted citation impact
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

18 citing papers in PubMed.

  1. Immature and mature myocardium in the pathophysiology of hypertrophic cardiomyopathy.Journal of molecular and cellular cardiology plus · 2026
    Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Pathophysiology of CaFrontiers in physiology · 2023
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. MMP9 inhibition increases autophagic flux in chronic heart failure.American journal of physiology. Heart and circulatory physiology · 2020
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Epigenetic regulation in heart failure.Current opinion in cardiology · 2016
    Review
  18. Crosstalk between Long Noncoding RNAs and MicroRNAs in Health and Disease.International journal of molecular sciences · 2016
    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

2 authors.

Shyam Sundar NandiDepartment of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, NE 68198, USA.
Paras Kumar MishraDepartment of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, NE 68198, USA ; Department of Anesthesiology, University of Nebraska Medical Center, Omaha, NE 68198, USA.

Funding

Inflammation, miRNA and autophagy in diabetesR01HL113281 · NHLBI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI MISHRA, PARAS KUMAR · 2013 to 2017
$1.9M
Exercise and H2S mitigate homocysteine-mediated beta2-adrenergic receptor dysfuncR01HL116205 · NHLBI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI MISHRA, PARAS KUMAR · 2013 to 2017
$1.9M
NHLBI NIH HHS R01 HL113281NHLBI NIH HHS R01 HL116205
6 · The paper itself

Abstract

Heart is the first organ formed during organogenesis. The fetal heart undergoes several structural and functional modifications to form the four-chambered mammalian heart. The adult heart shows different adaptations during compensatory and decompensatory heart failure. However, one common adaptation in the pathological heart is fetal reprogramming, where the adult heart expresses several genes and miRNAs which are active in the fetal stage. The fetal reprogramming in the failing heart raises several questions, such as whether the switch of adult to fetal genetic programming is an adaptive response to cope with adverse remodeling of the heart, does the expression of fetal genes protect the heart during compensatory and/or decompensatory heart failure, does repressing the fetal gene in the failing heart is protective to the heart? To answer these questions, we need to understand the expression of genes and miRNAs that are reprogrammed in the failing heart. In view of this, we provided an overview of differentially expressed genes and miRNAs, and their regulation in this review. Further, we elaborated novel strategies for a plausible future therapy of cardiovascular diseases.

Indexed as

fetal reprogrammingheart failuremiRNAremodelingtherapy

Identifiers

PMID25879081
PMCPMC4394627

What OpenQuestion holds

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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.