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October 27, 2024Development Growth & DifferentiationOpen Access

Transition from fetal to postnatal state in the heart: Crosstalk between metabolism and regeneration

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Key result

Postnatal metabolic transitions from glycolysis to fatty acid oxidation reduce cardiomyocyte proliferative capacity, but metabolic reprogramming offers potential for myocardial regeneration.

Why the study?

Adult myocardium has limited regenerative capacity after ischemic injury because cardiomyocytes rapidly lose their proliferative capacity postnatally, a decline closely linked to perinatal metabolic shifts.

Design

Review

Authors

TSTai SadaWKWataru KimuraKurume University

Discussion

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Implication

Limited adult cardiomyocyte proliferation impairs post-injury recovery; leaves open therapeutic targets to restore regeneration.

Structured PICO

P
Population
Mammalian cardiomyocytes (fetal and postnatal myocardium)

Understanding the postnatal metabolic transition in cardiomyocytes offers potential therapeutic targets for metabolic reprogramming to enhance myocardial regeneration after ischemic injury.

Cite This Study

Sada et al. (2024) conducted a review in Myocardial injury. Metabolic reprogramming was evaluated. Postnatal metabolic transitions from glycolysis to fatty acid oxidation reduce cardiomyocyte proliferative capacity, but metabolic reprogramming offers potential for myocardial regeneration.

synapsesocial.com/papers/6a7a1581e357fbdac5895b07https://doi.org/10.1111/dgd.12947
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