Cellular senescence is a permanent cell cycle arrest that plays a critical role in the development and pathogenesis of age-related diseases. This paper aims to present the biological mechanisms of cellular senescence and the role of the senescence-associated secretory phenotype (SASP) in the pathogenesis of atherosclerosis, as well as to discuss therapeutic strategies targeting senescent cells in cardiovascular diseases. Different types of cellular senescence are described, including replicative, stress-induced, and oncogene-induced senescence, along with the composition and regulation of SASP and its impact on chronic inflammation, endothelial dysfunction, vascular remodeling, and plaque destabilization. The involvement of senescent endothelial cells, vascular smooth muscle cells, and macrophages in the initiation and progression of atherosclerosis is also discussed. The paper reviews current research on senolytic and senomorphic therapies and highlights emerging approaches such as immunosenolytic and epigenetic interventions. The therapeutic potential of these strategies in reducing chronic vascular inflammation and improving plaque stability, as well as their limitations and challenges in clinical application, is emphasized.

Neurodegenerative diseases of the central nervous system, such as Alzheimer’s disease, Parkinson’s disease, and multiple sclerosis, represent a growing health challenge in ageing populations. Among the mechanisms underlying these disorders, increasing attention has been directed toward the role of cellular senescence. This process, triggered by chronic cellular and oxidative stress as well as DNA damage, leads to irreversible cell-cycle arrest and the development of the senescence-associated secretory phenotype (SASP). Within the central nervous system, the accumulation of senescent cells induces chronic inflammation, blood–brain barrier disruption, and progression of neurodegenerative processes. In this review, we present current evidence regarding the mechanisms of cellular senescence in the central nervous system, with particular emphasis on the role of SASP in neuroinflammation, vascular dysfunction, and neural tissue damage. Experimental and clinical data supporting the involvement of cellular senescence in the pathogenesis of Alzheimer’s disease, Parkinson’s disease, and multiple sclerosis are discussed. The review also covers methods for identifying senescent cells in the brain, including molecular marker-based approaches and machine learning-based tools. Importantly, we discuss the methodological limitations of commonly used senescence markers, such as their limited specificity and the risk of false-positive detection, particularly in the heterogeneous cellular environment of the central nervous system. Strategies to improve detection reliability discussed in this review include the use of multimarker signatures, analysis of SASP components using qRT-PCR and ELISA, as well as transcriptomic approaches such as RNA sequencing and single-cell RNA sequencing. Furthermore, we analyze therapeutic strategies targeting senescent cells—senolytics, senomorphics, and SASP modulation—together with their limitations and associated clinical challenges. The collected evidence indicates that precise characterization of senescent cell populations in the brain is essential for the development of disease-modifying therapies for neurodegenerative disorders.

Atrial septal defect (ASD) is characterized by an abnormal opening between the left (LA) and right atria (RA). Even though it’s one of the most prevalent congenital heart defects, there are still many knowledge gaps and clinical uncertainties. This review aims to create a complex description of ASD and discuss its link with pulmonary arterial hypertension (PAH). An extensive literature search was conducted on sites such as PubMed, Google Scholar, and ScienceDirect. This study reviews the key findings of peer-reviewed articles with the keywords ASD, PAH, and congenital heart defects. The research showed that whilst there are multiple reviews, there is still a need for a deeper understanding, especially in areas of embryology, decision thresholds for closure, and pediatric-specific long-term outcomes. Current guidelines often extrapolate data only from adults or avoid certain topics. Those ambiguities often lead to variable medical practices, missed opportunities, and uncertainty for families. This review is divided into clear sections, creating a step-by-step characterization of the most important information, which can be useful to specialists. It touches on important subjects and controversies. It shows a clear timeline, starting with embryology, genetics, and anatomy, through pathophysiology and patient description, ending with recommendations and indications for specific treatment methods. Moreover, it creates a clear connection between ASD and PAH, outlining its danger and the need for prevention.