Revisiting the Role of Autophagy in Cardiac Differentiation: A Comprehensive Review of Interplay with Other Signaling Pathways.

Autophagy is a critical biological process in which cytoplasmic components are sequestered in autophagosomes and degraded in lysosomes. This highly conserved pathway controls intracellular recycling and is required for cellular homeostasis, as well as the correct functioning of a variety of cellular differentiation programs, including cardiomyocyte differentiation. By decreasing oxidative stress and promoting energy balance, autophagy is triggered during differentiation to carry out essential cellular remodeling, such as protein turnover and lysosomal degradation of organelles. When it comes to controlling cardiac differentiation, the crosstalk between autophagy and other signaling networks such as fibroblast growth factor (FGF), Wnt, Notch, and bone morphogenetic proteins (BMPs) is essential, yet the interaction between autophagy and epigenetic controls remains poorly understood. Numerous studies have shown that modulating autophagy and precisely regulating it can improve cardiac differentiation, which can serve as a viable strategy for generating mature cardiac cells. These findings suggest that autophagy should be studied further during cardiac differentiation. The purpose of this review article is not only to discuss the relationship between autophagy and other signaling pathways that are active during the differentiation of cardiomyocytes but also to highlight the importance of manipulating autophagy to produce fully mature cardiomyocytes, which is a tough challenge.

Comparison of left ventricular systolic function by 2D speckle-tracking echocardiography between normal pregnant women and pregnant women with preeclampsia.

Introduction: In light of previous studies reporting the significant effects of preeclampsia on cardiac dimensions, we sought to evaluate changes in the left ventricular (LV) systolic and diastolic functions in patients with preeclampsia with a view to investigating changes in cardiac strain. Methods: This cross-sectional study evaluated healthy pregnant women and pregnant women suffering from preeclampsia who were referred to our hospital for routine healthcare services. LV strain was measured by 2D speckle-tracking echocardiography. Results: Compared with the healthy group, echocardiography in the group with preeclampsia showed a significant increase in the LV end-diastolic diameter (47.43 ± 4.94 mm vs 44.84 ± 4.30 mm; P = 0.008), the LV end-systolic diameter (31.16 ± 33.3 mm vs 29.20 ± 3.75 mm; P = 0.008), and the right ventricular diameter (27.93 ± 1.71 mm vs 24.53 ± 23.3; P = 0.001). The mean global longitudinal strain was -18.69 ± 2.8 in the group with preeclampsia and -19.39 ± 3.49 in the healthy group, with the difference not constituting statistical significance (P = 0.164). The mean global circumferential strain in the groups with and without preeclampsia was -20.4 ± 12.4 and -22.68 ± 5.50, respectively, which was significantly lower in the preeclampsia group (P = 0.028). Conclusion: The development of preeclampsia was associated with an increase in the right and left ventricular diameters, as well as a decrease in the ventricular systolic function, demonstrated by a decline in global circumferential strain.