Level D· Scientific groundwork from lab and animal studiesNarrative ReviewEurope PMCOpen access

Recent Insights into Endogenous Mammalian Cardiac Regeneration Post-Myocardial Infarction

Fiorino E., Rossin D., Vanni R., Aubry M., Giachino C., Rastaldo R.

Narrative Review on Cardiovascular Disease, published in Int J Mol Sci (2024) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • 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
Narrative Review
Journal
Int J Mol Sci (2024)
Reported sample size
—
Source database
Europe PMC
PMID
39519298
PMCID
PMC11546116
DOI
10.3390/ijms252111747
Citations
8

Abstract (original English)

Myocardial infarction (MI) is a critical global health issue and a leading cause of heart failure. Indeed, while neonatal mammals can regenerate cardiac tissue mainly through cardiomyocyte proliferation, this ability is lost shortly after birth, resulting in the adult heart's inability to regenerate after injury effectively. In adult mammals, the adverse cardiac remodelling, which compensates for the loss of cardiac cells, impairs cardiac function due to the non-contractile nature of fibrotic tissue. Moreover, the neovascularisation after MI is inadequate to restore blood flow to the infarcted myocardium. This review aims to synthesise the most recent insights into the molecular and cellular players involved in endogenous myocardial and vascular regeneration, facilitating the identification of mechanisms that could be targeted to trigger cardiac regeneration, reduce fibrosis, and improve functional recovery post-MI. Reprogramming adult cardiomyocytes to regain their proliferative potential, along with the modulation of target cells responsible for neovascularisation, represents promising therapeutic strategies. An updated overview of endogenous mechanisms that regulate both myocardial and coronary vasculature regeneration-including stem and progenitor cells, growth factors, cell cycle regulators, and key signalling pathways-could help identify new critical intervention points f

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is a narrative review: it collects no new patient data and does not systematically appraise evidence quality.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

How we grade evidence
MyocardiumHeartMyocytes, CardiacAnimalsHumansMyocardial InfarctionRegenerationSignal TransductionNeovascularization, Physiologic

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