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Myocyte Proliferation

Di: Everly

神经元可以调节靶器官的发育、发病机制和再生。然而，神经元在心脏发育和再生过程中的作用仍不清楚。我们在体内通过基因抑制交感神经支配，导致心脏扩大，心肌细胞数量增加。转录组

All these mechanisms play a role in cardiac morphogenesis, but experimental studies have shown that the major determinant of cardiac size during prenatal development is myocyte proliferation.

Mitochondria regulate proliferation in adult cardiac myocytes

Hopx and Hdac2 Interact to Modulate Gata4 Acetylation and Embryonic ...

To (re)initiate cardiac myocyte proliferation in adult mammalian hearts, a thorough understanding of the molecular circuitry governing cardiac myocyte cell cycle regulation is

A recent study suggests that systemic hypoxemia in adult male mice can induce cardiac myocytes to proliferate.

  • Myocyte Proliferation and Ventricular Remodeling
  • Myocyte proliferation in end-stage cardiac failure in humans
  • Nerves Regulate Cardiomyocyte Proliferation and Heart Regeneration

Improvement in the methodological approach to the analysis of the myocardium has provided clear evidence of cardiac myocyte proliferation, questioning the general belief that the growth

Cardiomyocyte proliferation and regeneration are key to the functional recovery of myocardial tissue from injury. In the recent years, studies on cardiomyocyte proliferation overturned the

Myocyte replication occurs in the failing human heart, 1 and this form of cell growth tends to compensate for the exhaustion of myocyte hypertrophy. 2 In chronic heart failure,

The addition of newly generated myocytes leads to cavitary dilation with relative thinning of the wall. Conversely, myocyte proliferation, characterized by the parallel addition of cells, can be

Follistatin From hiPSC-Cardiomyocytes Promotes Myocyte Proliferation in Pigs With Postinfarction LV Remodeling Circ Res. 2025 Jan 17;136(2):161-176. doi:

Cardiomyocyte proliferation as a promising strategy for repairing cardiac function requires an urgent understanding of the molecular mechanisms targeting immune cell

All these mechanisms play a role in cardiac morphogenesis, but experimental studies have shown that the major determinant of cardiac size during prenatal development is myocyte proliferation.

EVs secreted by C-MSCs with Notch1 deletion were not effective in preventing apoptosis and myocyte proliferation and angiogenesis. It appears from the proteomic profile

In the heart, the ability of cardiac myocytes (CM) to proliferate decreases gradually after birth and becomes almost non-existent weeks after birth. Adult myocytes undergo terminal differentiation

Hirai, M., Chen, J. & Evans, S. M. Tissue-specific cell cycle indicator reveals unexpected findings for cardiac myocyte proliferation. Circ. Res. 118, 20–28 (2016). Article

With regard to the cellular sources of myocyte turnover, cardiomyocyte proliferation has emerged as the dominant mechanism of myocyte replenishment in the injured

These findings provide the theoretical basis of targeting cellular fate plasticity to induce cardiomyocyte proliferation or formation, and also provide the clues for stimulating heart

Keywords: Cardiac myocyte, proliferation, regeneration, developmental biology. Too often, the heart does not have the capacity to overcome loss of cardiac muscle cells after injury, thus

Interestingly, a phorbol ester had a similar effect on myocyte proliferation. Furthermore, 1,25(OH)2D3 increased myocyte protein levels and increased cell size, suggesting that it

Foxp1 mutant embryos have severe defects in cardiac morphogenesis, including outflow tract septation and cushion defects, a thin ventricular myocardial compact zone caused by defects

The intact heart undergoes complex and multiscale remodelling processes in response to altered mechanical cues. Remodelling of the myocardium is regulated by a

More specifically, a recent study investigated the effects of hypoxemia on myocyte proliferation in adult mammals. Gradual reduction of ambient oxygen levels to 7% oxygen induced a proliferative response in

Newborn mammalian cardiomyocytes quickly transition from a fetal to an adult phenotype that utilizes mitochondrial oxidative phosphorylation but loses mitotic capacity. We

Here, we show using transgenic zebrafish that inhibition of cardiac innervation leads to reduction of myocyte proliferation following injury. Specifically, pharmacological

While some mechanisms apply to cell proliferation and differentiation in general, much of the regulations are tissue-specific, significantly increasing the complexity of

In ischemic hearts with RISP deletion, new cardiomyocytes migrated into the infarcted region, suggesting the potential for therapeutic cardiac regeneration. RNA

We report here by confocal microscopy that 14 myocytes per million were in mitosis in control human hearts. A nearly 10-fold increase in this parameter was measured in end

Genetic ablation of periostin in HCM mice reduced but did not extinguish non-myocyte proliferation and fibrosis. In contrast, administration of Tgf-β-neutralizing antibodies abrogated