Biomedicines

Endometriosis represents a prevalent gynaecological disorder, impacting around 10% of the female population and affecting as many as 50% of women who are facing challenges with infertility. The pathogenesis of the disease encompasses intricate processes such as the formation of adhesions, degradation of the extracellular matrix, angiogenesis, increased cell proliferation, impaired apoptosis, and dysregulation of the immune response. Although endometriosis is common, its precise etiology remains unidentified, despite various hypotheses being suggested. Recent findings underscore the significance of non-coding RNAs, specifically long non-coding RNAs (lncRNAs) and microRNAs (miRNAs), which have been identified as important regulators in the development of endometriosis. This literature review integrates findings from various transcriptomic and molecular studies to distinguish between lncRNAs and miRNAs that are associated with direct pathogenic roles and those that simply represent altered gene expression profiles in endometriosis. Particular long non-coding RNAs, such as H19, MALAT1, and LINC01116, are associated with chromatin remodeling, functioning as competitive endogenous RNAs, and influencing critical signaling pathways. Concurrently, specific microRNAs, including the miR-200 family, miR-145, and let-7b, seem to govern processes like epithelial-to-mesenchymal transition, angiogenesis, and cell adhesion. The findings highlight the significant potential of non-coding RNAs to serve as biomarkers for diagnostic purposes and as innovative therapeutic targets. Subsequent research endeavours ought to focus on corroborating these findings and elucidating the specific pathogenic roles of these non-coding RNAs in the context of endometriosis.

Over the past decade, interest has grown in understanding the morphofunctional changes that mesenchymal stem cells (MSCs) undergo due to age-associated senescence—a process particularly relevant given that adults and elderly individuals are the primary candidates for regenerative therapies. This study addresses this knowledge gap by systematically analyzing the influence of age-related senescence on the morphofunctional properties of MSCs derived from the oral cavity. A scoping review was conducted following the PRISMA-ScR guidelines. The databases searched were MEDLINE, SCOPUS, and Web of Science. In vitro studies were included if their primary objective was to investigate oral cavity mesenchymal stromal cells and age-related senescence. A total of 455 studies were identified, of which 17 were selected. Studies on MSCs from the oral cavity have shown that age-related senescence, starting around 35 years, reduces proliferation, viability, clonogenic capacity, and differentiation potential—particularly toward osteogenic and chondrogenic lineages—with higher values observed in younger individuals. However, MSC surface markers remain stably expressed and show no association with aging. Some studies also report no significant differences in proliferation rate or cell doubling time at early passages, and MSCs retain some plasticity at these stages. Despite age-related limitations, oral MSCs from elderly donors remain a promising therapeutic source, especially at early in vitro passages. Further research is needed to explore innovative strategies to enhance the regenerative potential of oral MSCs from older donors.

Hepatorenal syndrome (HRS) is a high-mortality, potentially reversible form of kidney failure that arises from a tight hemodynamic–inflammatory coupling in cirrhosis. Contemporary redefinitions prioritize creatinine kinetics over static thresholds and recognize non-acute kidney injury (AKI) functional phenotypes, enabling earlier recognition but heightening the need for precise etiologic triage. This narrative synthesis integrates current concepts across pathophysiology, diagnosis and management. Portal hypertension, bacterial translocation and inflammatory mediators amplify splanchnic vasodilation and effective arterial underfilling. Compensatory neurohumoral activation precipitates renal vasoconstriction, intrarenal microcirculatory dysfunction and sodium–water retention. The pivotal diagnostic fork remains HRS–AKI versus acute tubular necrosis. A pragmatic, tiered strategy, structured volume assessment, filtration markers and a parsimonious tubular-injury panel offer actionable discrimination, whereas fractional excretion indices serve as adjuncts only. Initial therapy should be bundled and time-sensitive: remove nephrotoxins, treat infection and initiate albumin plus a vasoconstrictor. The transplant strategy should default to isolated liver transplantation unless end-stage renal disease is established. Future priorities include validated biomarker cut-offs, ultrasound-guided volume algorithms and pathway-based trials to reduce diagnostic delay and improve survival.