Evidence map›Paper›PMID 24905188›Full record

ReviewCanadian journal of physiology and pharmacology2014

Dysregulation of Mfn2 and Drp-1 proteins in heart failure.

Srikanth Givvimani, Sathnur Pushpakumar, Sudhakar Veeranki, Suresh C Tyagi

Abstract readReview
In one paragraph

Review in Canadian journal of physiology and pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
3.6field-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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Genetic mutations in kinases: a comprehensive review on marketed inhibitors and unexplored targets in Parkinson's disease.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
    Review
  8. Review
  9. Article
  10. A Need to Preserve Ejection Fraction during Heart Failure.International journal of molecular sciences · 2024
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article
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.

Srikanth GivvimaniDepartment of Physiology & Biophysics, School of Medicine, University of Louisville, KY 40202, USA.
Sathnur Pushpakumar
Sudhakar Veeranki
Suresh C Tyagi
University of Louisville · US

Funding

Reversing diabetic muscle myopathy by exercise and exosomesR01HL074185 · NHLBI · UNIVERSITY OF LOUISVILLE · PI TYAGI, SURESH C. · 2003 to 2018
$5.7M
Mechanisms of Homocysteine-Induced Fibrinogen-Amyloid Plaque FormationR01NS084823 · NINDS · UNIVERSITY OF LOUISVILLE · PI LOMINADZE, DAVID, TYAGI, SURESH C. · 2013 to 2017
$2.7M
Mitophagic and anti-angiogenic mechanism of heart failureR01HL108621 · NHLBI · UNIVERSITY OF LOUISVILLE · PI TYAGI, SURESH C. · 2011 to 2015
$1.8M
NHLBI NIH HHS R01 HL074185NHLBI NIH HHS R01 HL108621NINDS NIH HHS R01 NS084823
6 · The paper itself

Abstract

Therapeutic approaches for cardiac regenerative mechanisms have been explored over the past decade to target various cardiovascular diseases (CVD). Structural and functional aberrations of mitochondria have been observed in CVD. The significance of mitochondrial maturation and function in cardiomyocytes is distinguished by their attribution to embryonic stem cell differentiation into adult cardiomyocytes. An abnormal fission process has been implicated in heart failure, and treatment with mitochondrial division inhibitor 1 (Mdivi-1), a specific inhibitor of dynamin related protein-1 (Drp-1), has been shown to improve cardiac function. We recently observed that the ratio of mitofusin 2 (Mfn2; a fusion protein) and Drp-1 (a fission protein) was decreased during heart failure, suggesting increased mitophagy. Treatment with Mdivi-1 improved cardiac function by normalizing this ratio. Aberrant mitophagy and enhanced oxidative stress in the mitochondria contribute to abnormal activation of MMP-9, leading to degradation of the important gap junction protein connexin-43 (Cx-43) in the ventricular myocardium. Reduced Cx-43 levels were associated with increased fibrosis and ventricular dysfunction in heart failure. Treatment with Mdivi-1 restored MMP-9 and Cx-43 expression towards normal. In this review, we discuss mitochondrial dynamics, its relation to MMP-9 and Cx-43, and the therapeutic role of fission inhibition in heart failure.

Indexed as

AnimalsConnexin 43DynaminsGTP PhosphohydrolasesHeart FailureHumansMatrix Metalloproteinase 9Microtubule-Associated ProteinsMitochondrial DynamicsMitochondrial ProteinsQuinazolinones3-(2,4-dichloro-5-methoxyphenyl)-2-sulfanyl-4(3H)-quinazolinoneConnexin 43DNM1L protein, humanDynaminsGTP PhosphohydrolasesMatrix Metalloproteinase 9MFN2 protein, humanMicrotubule-Associated ProteinsMitochondrial ProteinsQuinazolinonesCx-43Drp-1fission mitochondrialefusioninsuffisance cardiaque par surcharge de pressionMfn2mitochondrial fissionMMP-9pressure overload heart failure

Identifiers

PMID24905188
PMCPMC4228691
OpenAlexW1999931656

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.