Ventricular trabeculation and compaction are two of the many essential steps for generating a functionally competent ventricular wall. A significant reduction in trabeculation is usually associated with ventricular compact zone deficiencies (hypoplastic wall), which commonly leads to embryonic heart failure and early embryonic lethality. In contrast, hypertrabeculation and lack of ventricular wall compaction (noncompaction) are closely related defects in cardiac embryogenesis associated with left ventricular noncompaction (LVNC), a genetically heterogenous disorder. Here we summarize our recent findings through the analyses of several genetically engineered mouse models that have defects in cardiac trabeculation and compaction. Our data indicate that cellular growth and differentiation signaling pathways are keys in these ventricular morphogenetic events.During mammalian embryonic heart development, the ventricles undergo a series of morphogenesis [1][2][3]. Ventricular trabeculation and compaction are two of the many essential steps for generating a functionally competent ventricular wall [4]. Simplistically, development of the ventricular wall has 4 distinct stages; Stage 1, formation of single cell layered myocardium at an early developmental stage: Following induction via adjacent endoderm, lateral mesoderm gives rise to an early tubular heart. The heart at this stage is composed of one cell layer of myocardium and one cell layer of endocardium lining the lumen [1,5]; Stage 2, formation of a trabeculated and compact myocardium at early midgestation stage: As the myocardium thickens, cardiomyocytes along the inner wall form sheet-like protrusions into the lumen to give rise to trabecular myocardium, while the outside layer of myocardium becomes organized into compact myocardium. Ventricular trabeculation has been suggested to facilitate oxygen and nutrient exchange and to enhance force generation to match the increasing blood flow in the developing embryos [1,4]; Stage 3, myocardial compaction at late midgestation stage: As development proceeds, the trabecular myocardium becomes compacted towards the myocardial wall and contributes to forming a thicker, compact ventricular wall. The majority of trabeculae have become compacted after E14.5 in mouse embryos [4,6]; Stage 4, Formation of a mature and multilayered spiral myocardium during late fetal and neonatal stage [2,7]. Following the formation of primitive trabecular ridges (about E9.5 in mouse embryo, start of stage 2), the myocardium undergoes extensive expansion by either recruiting cardiomyocytes from myocardial wall into the trabecular ridges or via cellular proliferation within the trabecular cardiomyocytes. In support of the cellular recruitment mechanism, proliferative activity is consistently higher within the compact myocardium as there is a gradient of decreasing proliferation and increased differentiation from the outside of the heart towards the lumen and trabeculae side [8][9][10][11]. This balance of proliferation and differentiation is...
Per retrieved oocyte, a nearly threefold higher dose of FSH had to be administered when ovarian stimulation had been initiated in the luteal phase. Furthermore, the present study casts doubt on the efficacy of initiating ovarian stimulation in the luteal phase in terms of pregnancy achievement. Thus, this concept is currently not feasible for routine use, and it should also be explored further before using it at larger scale in the context of emergency stimulation for fertility preservation.
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