Evidence map›Paper›PMID 24055000›Full record

ReviewBiochimica et biophysica acta2013

Cardiac matrix: a clue for future therapy.

Paras Kumar Mishra, Srikanth Givvimani, Vishalakshi Chavali, Suresh C Tyagi

Open access · greenAbstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

34 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
  2. Dipeptidyl peptidase-4 deficiency prevents chronic stress-induced cardiac remodeling and dysfunction in mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. Extracellular Matrix in Regulation of Contractile System in Cardiomyocytes.International journal of molecular sciences · 2019
    Review
  12. TFAM overexpression reduces pathological cardiac remodeling.Molecular and cellular biochemistry · 2019
    Article
  13. Review
  14. The Role of Osteoprotegerin and Its Ligands in Vascular Function.International journal of molecular sciences · 2019
    Review
  15. Review
  16. Review
  17. Article
  18. Targeting miRNA for Therapy of Juvenile and Adult Diabetic Cardiomyopathy.Advances in experimental medicine and biology · 2018
    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

4 authors at 2 institutions in 1 country.

Paras Kumar MishraDepartment of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, NE 68198, USA.
Srikanth Givvimani
Vishalakshi Chavali
Suresh C Tyagi
University of Louisville Hospital · USUniversity of Nebraska Medical Center · US

Funding

Reversing diabetic muscle myopathy by exercise and exosomesR01HL074185 · NHLBI · UNIVERSITY OF LOUISVILLE · PI TYAGI, SURESH C. · 2003 to 2018
$5.7M
Inflammation, miRNA and autophagy in diabetesR01HL113281 · NHLBI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI MISHRA, PARAS KUMAR · 2013 to 2017
$1.9M
Mitophagic and anti-angiogenic mechanism of heart failureR01HL108621 · NHLBI · UNIVERSITY OF LOUISVILLE · PI TYAGI, SURESH C. · 2011 to 2015
$1.8M
NHLBI NIH HHS HL-108621NHLBI NIH HHS HL-113281NHLBI NIH HHS HL-74185NHLBI NIH HHS R01 HL074185NHLBI NIH HHS R01 HL108621NHLBI NIH HHS R01 HL113281
6 · The paper itself

Abstract

Cardiac muscle is unique because it contracts ceaselessly throughout the life and is highly resistant to fatigue. The marvelous nature of the cardiac muscle is attributed to its matrix that maintains structural and functional integrity and provides ambient micro-environment required for mechanical, cellular and molecular activities in the heart. Cardiac matrix dictates the endothelium myocyte (EM) coupling and contractility of cardiomyocytes. The matrix metalloproteinases (MMPs) and their tissue inhibitor of metalloproteinases (TIMPs) regulate matrix degradation that determines cardiac fibrosis and myocardial performance. We have shown that MMP-9 regulates differential expression of micro RNAs (miRNAs), calcium cycling and contractility of cardiomyocytes. The differential expression of miRNAs is associated with angiogenesis, hypertrophy and fibrosis in the heart. MMP-9, which is involved in the degradation of cardiac matrix and induction of fibrosis, is also implicated in inhibition of survival and differentiation of cardiac stem cells (CSC). Cardiac matrix is distinct because it renders mechanical properties and provides a framework essential for differentiation of cardiac progenitor cells (CPC) into specific lineage. Cardiac matrix regulates myocyte contractility by EM coupling and calcium transients and also directs miRNAs required for precise regulation of continuous and synchronized beating of cardiomyocytes that is indispensible for survival. Alteration in the matrix homeostasis due to induction of MMPs, altered expression of specific miRNAs or impaired signaling for contractility of cardiomyocytes leads to catastrophic effects. This review describes the mechanisms by which cardiac matrix regulates myocardial performance and suggests future directions for the development of treatment strategies in cardiovascular diseases.

Indexed as

AnimalsCardiovascular DiseasesExtracellular MatrixHumansMatrix MetalloproteinasesMyocardiumMyocytes, CardiacTissue Inhibitor of MetalloproteinasesMatrix MetalloproteinasesTissue Inhibitor of Metalloproteinasesacute pulmonary thromboembolismAngiogenesisAPTcardiac progenitor cellcardiac stem cellcardiovascular diseaseCPCCSCCVDDNA methyl transferaseDNMTECMextracellular matrixHeartmatrix metalloproteinaseMicroRNAmiRNAMMPreactive oxygen speciesROSsarco endoplasmic reticulum ca(2+)ATPaseSERCAStem cellTIMPtissue inhibitor of MMPvascular endothelial growth factorVEGF

Identifiers

PMID24055000
PMCPMC4111554
OpenAlexW2026949272

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.