Gestational complications, such as preeclampsia and gestational diabetes mellitus (GDM), pose significant risks to maternal and fetal health and increase long-term cardiovascular disease risk in offspring. This review aims to synthesize current knowledge on the roles of ferroptosis and neutrophil extracellular trap formation (NETosis)—two regulated cell death pathways—in these pregnancy-related conditions. We performed a comprehensive analysis of preclinical and clinical studies that investigate the involvement of dysregulated iron metabolism, oxidative stress, inflammation, and endothelial dysfunction mediated by ferroptosis and NETosis in gestational pathologies. Evidence indicates that disturbances in maternal iron homeostasis and enhanced formation of lipid peroxides and NETs contribute to placental dysfunction and systemic inflammation, exacerbating disease severity. Therapeutic strategies targeting these pathways are emerging but require further validation. Our review also identifies key gaps in mechanistic understanding, biomarker development, and translational research needs. We conclude that modulation of ferroptosis and NETosis offers promising avenues for improving diagnosis and treatment of pregnancy complications, though carefully designed clinical studies are essential to confirm their clinical utility and safety.

Heart Failure with Preserved Ejection Fraction (HFpEF) is an increasingly prevalent clinical syndrome that poses a significant public health challenge due to its complex pathophysiology, diagnostic limitations, and lack of effective therapies. Central to its development are multifactorial and interrelated mechanisms, including left ventricular diastolic dysfunction, myocardial fibrosis, inflammation, endothelial dysfunction, and cardiomyocyte hypertrophy. In recent years, noncoding RNAs (ncRNAs)—particularly microRNAs (miRNAs) and long noncoding RNAs (LncRNAs)—have emerged as critical regulators of these cellular and molecular pathways. This review outlines the major pathophysiological mechanisms underlying HFpEF and highlights the noncoding RNAs most extensively studied in this context. Several ncRNAs have shown promise as biomarkers for the diagnosis and prognosis of HFpEF, owing to their tissue specificity, stability in circulation, and involvement in disease-relevant pathways. However, their integration into routine clinical practice remains limited. Importantly, the regulatory functions of ncRNAs in HFpEF pathophysiology also position them as potential therapeutic targets. Early experimental studies demonstrate encouraging results, suggesting that ncRNA-targeted interventions may support the development of personalized treatment strategies tailored to the diverse clinical phenotypes observed in HFpEF.

Background: Titin (TTN), a giant structural and signaling protein of striated muscle, participates in intracellular signaling networks and cytoskeletal organization, potentially influencing cell activation, trafficking, and interactions with other tissues, including the heart. Methods: In this pilot study, 29 patients with acute myocarditis and 10 healthy individuals were prospectively enrolled. Peripheral blood was obtained on the first day of hospital admission, total RNA was isolated from peripheral blood mononuclear cells (PBMCs), and TTN mRNA expression was quantified. Results: TTN expression in PBMCs was significantly higher in patients with acute myocarditis compared with healthy controls (p = 0.015), corresponding to a 2.8-fold median increase. Moreover, TTN expression showed a strong positive correlation with global longitudinal strain impairment (Spearman’s r = 0.576, p < 0.001), a moderate positive correlation with peak hs-cTnI levels (r = 0.435, p = 0.021; and a moderate inverse correlation with baseline LVEF (r = −0.421, p = 0.025). Conclusions: These findings support a pathophysiological link between TTN-related pathways in peripheral immune cells and myocardial injury in acute myocarditis and raise the hypothesis that TTN expression in PBMCs may serve as a novel biomarker of disease severity and long-term ventricular remodeling. Further studies in larger cohorts are warranted to validate these results and to elucidate the mechanistic role of titin in immune–cardiac cross-talk.