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Neonatal (1 d)KI67 good nuclei; apoptosis; LV binucleation; volume proliferative index Neonatal (1 d)KI67 positive nuclei; apoptosis; LV binucleation; volume proliferative index[98,100] [93]J. Clin. Med. 2021, ten,eight ofTable 1. Cont. Model GC Timing of Exposure Route Duration of Exposure SC Age of Evaluation Fetal (21 d Pc) to Adulthood (up to 24 w) Cardiac Effects Cardiomyocyte Characteristics N/A Ref.RatDEXLate (151 d Computer)MiceGR KOFetalN/AFetal (E 17.5 d)calreticulin protein expression (fetal); calsequestrin protein expression (fetal); calreticulin protein expression (adulthood) heart size; ventricular volume; impaired cardiac function; short, disorganized myofibrils; myofibrils fail to align within the myocardium[106]N/A[92]Neonatal mouse CMCORTTreated for 24 hIn vitroFetalN/Acontractility; Zdisc assembly; sarcomere length; look of mature myofibrils; mitochondrial activity; contraction relaxation events[91]BETA, betamethasone; CM, cardiomyocyte; CORT, corticosterone; d, day; d GA, days of gestational age; d Pc, days postconception; DEX, dexamethasone; E, embryonic; GC, glucocorticoid; GR KO, glucocorticoid receptor knockout; h, hours; HC, hydrocortisone; IC, intracoronary; IM, intramuscular; IV, intravenous; IVS, interventricular septum; LV, left ventricle; m, months; N/A, not applicable; RV, proper ventricle; SC, subcutaneous; w, weeks; y, years; , increase; , lower; , no alter.J. Clin. Med. 2021, ten,9 ofLate gestational cortisol infusion in sheep increases blood stress, fetal heart to body weight ratio, left ventricular cardiomyocyte size, and cardiac angiotensinogen mRNA: these outcomes are constant with accelerated cardiovascular maturation mediated by glucocorticoid exposure [97]. The hypertrophic growth in left ventricular cardiomyocytes is potentially a physiological response to the increase in blood stress and cardiac angiotensinogen mRNA levels [97]. Reini and colleagues [102] reported a similar elevated fetal heart to body weight ratio and improved ventricular wall thickness right after cortisol infusion in late gestation. Having said that, the morphological cardiac modifications weren't resulting from adjustments in blood stress or cardiac fibrosis, suggesting overexposure to cortisol in fetal sheep directly influenced cardiomyocyte growth by acting around the cardiac mineralocorticoid and glucocorticoid receptors [102]. Inside a model of maternal pressure, fetal sheep chronically exposed to maternally administered cortisol throughout late gestation exhibited relatively bigger heart to physique weight ratios, elevated ventricular wall thickness, and enhanced imply arterial blood pressure [95]. Interestingly, augmented cardiac development was attributed to an accelerated hyperplastic growth of cardiomyocytes, evidenced by an improved proportion of cardiomyocytes stained optimistic for Ki67 and no modify in cardiomyocyte size [95]. Improved maternal cortisol levels during late gestation by cortisol infusion also stimulated both proliferation and apoptosis within the fetal sheep hearts [103]. Clearly, chronic exposure to maternal cortisol triggers cardiac remodelling and altered development trajectory during the crucial maturational transition period for cardiomyocytes. Inside a fetal Ne, the brain can method only a fraction for the reason that of its growthrestricted model (danger element for preterm birth), betamethasoneexposed sheep fetuses showed elevated relative heart weight and exhibited enhanced left ventricular responsiveness to adrenoceptor stimulation, which may perhaps result in cardiac dysCs of six different muscle tissues (longissimus thoracis et lumborum, biceps femoris function [105]. Cardiac function is highly dependent around the electrical activity of cardiomyocytes and their ability to propagate.