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  1. 1 paź 2021 · Myocardial infarction and cardiac pressure overload induce regional patterns of cycling cardiomyocytes. Mechanistically, cardiomyocyte cell cycle activity requires the Hippo pathway...

  2. 22 mar 2018 · In vivo lineage tracing revealed that 15%–20% of adult cardiomyocytes expressing the four factors underwent stable cell division, with significant improvement in cardiac function after acute or subacute myocardial infarction. Chemical inhibition of Tgf-β and Wee1 made CDK1 and cyclin B dispensable.

  3. 22 mar 2018 · We screened cell-cycle regulators expressed in proliferating fetal cardiomyocytes and found that overexpression of cyclin-dependent kinase 1 (CDK1), CDK4, cyclin B1, and cyclin D1 efficiently induced cell division in post-mitotic mouse, rat, and human cardiomyocytes.

  4. 27 sty 2021 · First, residual cardiomyocytes in damaged hearts re-enter the cell cycle to acquire the proliferative capacity by the modifications of cell cycle-related genes or regulation of growth-related...

  5. 28 wrz 2018 · Key points. Clonal analysis shows that two myocardial cell lineages, which segregate early at gastrulation, form the heart, with cell sublineages contributing to the arterial and venous poles,...

  6. 6 kwi 2021 · Here, we review both the classical and recent literature on the molecular and cellular mechanisms underlying heart regeneration, with a particular focus on how injury triggers the cell-cycle re-entry of quiescent cardiomyocytes to replenish their massive loss after myocardial infarction or ventricular resection.

  7. 1 mar 2024 · Ybx1,miR-214. Nfix induces Ybx1 degradation through ubiquitination, represses cyclin A2 and cyclin B1 expression, and inhibits cardiomyocyte proliferation. In addition, Nfix adsorbes miR-214, promotes the expression of Gsk3β, inhibites β-catenin activity, and arrests cardiomyocyte proliferation.

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