Level B· Emerging clinical evidence with positive signalsClinical TrialEurope PMC

Angiogenesis in the infarcted myocardium

Cochain C., Channon KM., Silvestre JS.

Clinical Trial on Cardiovascular Disease, published in Antioxid Redox Signal (2013) — summary generated from the PubMed abstract.

Open my reading list
Level B· Emerging clinical evidence with positive signalsEvidence level of this study

Several human studies show positive signals, while research methods and sample sizes continue to develop.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
Read the A–D evidence level guide

This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Clinical Trial
Journal
Antioxid Redox Signal (2013)
Reported sample size
—
Source database
Europe PMC
PMID
22870932
PMCID
PMC3567783
DOI
10.1089/ars.2012.4849
Citations
195

Abstract (original English)

Significance Proangiogenic therapy appeared a promising strategy for the treatment of patients with acute myocardial infarction (MI), as de novo formation of microvessels, has the potential to salvage ischemic myocardium at early stages after MI, and is also essential to prevent the transition to heart failure through the control of cardiomyocyte hypertrophy and contractility. Recent advances Exciting preclinical studies evaluating proangiogenic therapies for MI have prompted the initiation of numerous clinical trials based on protein or gene transfer delivery of growth factors and administration of stem/progenitor cells, mainly from bone marrow origin. Nonetheless, these clinical trials showed mixed results in patients with acute MI. Critical issues Even though methodological caveats, such as way of delivery for angiogenic growth factors (e.g., protein vs. gene transfer) and stem/progenitor cells or isolation/culture procedure for regenerative cells might partially explain the failure of such trials, it appears that delivery of a single growth factor or cell type does not support angiogenesis sufficiently to promote cardiac repair. Future directions Optimization of proangiogenic therapies might include stimulation of both angiogenesis and vessel maturation and/or the use of additional sources of stem/progenitor cells, such as cardiac progenitor cells. Experimental unraveling o

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.

Evidence level

Several human studies show positive signals, while research methods and sample sizes continue to develop.

How we grade evidence
MicrocirculationCapillariesEndothelial CellsMyocytes, CardiacAnimalsHumansMiceMyocardial InfarctionReperfusion InjuryIntercellular Signaling Peptides and Proteins

Browse all related research

Filter the research library by this study's title keywords, author, or publication year.

Related research