Abstract. Foam cells play a crucial role in the initiation and progression of atherosclerosis, a condition marked by the development and growth of plaques that narrow blood vessel lumens. This narrowing can prevent normal blood flow and, in severe cases, lead to plaque rupture and blood clot formation, which can cause brain stroke or myocardial infarction. The origin of foam cells is diverse, arising from monocytes, vascular smooth muscle cells, stem/progenitor cells, dendritic and endothelial cells. The foam cells attempt to eliminate excess lipoproteins and cholesterol, thus inadvertently contributing to plaque development and rupture. Cholesterol uptake, efflux, and esterification are the major processes regulating foam cell formation. Advances in technology, such as identification of cell-surface markers for lineage tracing and single-cell RNA sequencing, have unveiled diverse molecular mechanisms involved in the formation of foam cells from different origins, offering new insights into plaque formation and potential targets for anti-foam cell therapies. In this review, we focus on the inhibitory effects of medicinal plants and their bioactive components on foam cell formation. Various mechanisms are explored, including the inhibition of cholesterol uptake and up-regulation of cholesterol efflux, as well as the suppression of inflammatory and adhesion activities. Emphasising a cellular target-based therapeutic approach, this review envisions the development of innovative plant-based medications for atherosclerosis treatment.

This review offers an in-depth analysis of mitochondrial DNA (mtDNA) mutations in colorectal cancer stem cells (CSCs), emphasizing their significant impact on tumor dynamics and potential therapeutic strategies. Key topics include the identification and properties of CSCs in colorectal cancer, the distinctive features of the mitochondrial genome, and the functional consequences of mtDNA mutations. The review hypothesizes that CSCs rely on well-functioning mitochondria for crucial aspects like energy production, yet mtDNA mutations can lead to mitochondrial dysfunction, altering CSC characteristics and influencing cancer progression. The article discusses emerging therapeutic approaches targeting mitochondrial function in colorectal CSCs and highlights the need for advanced research, including the development of preclinical models and exploration of targeted therapies, to improve understanding and treatment of colorectal cancer.

Background: The escalating global burden of stress and depression underscores an urgent need to unravel their complex interrelationships and underlying mechanisms. This investigation delves into the intricate dynamics between stress and depression, spotlighting the Neuroimmunoinflammatory Stress Model (NIIS) that elucidates the pivotal role of cellular and molecular pathways in mediating these conditions. Methods: Through an exhaustive review of literature spanning epidemiology, neurobiology, and psychoneuroimmunology, this study synthesizes current understandings of stress and depression. It accentuates their definitional scopes, interplay, and the intricacies of the NIIS model, which integrates neuroimmune-inflammatory responses into the conceptual framework of stress-depression interaction. Results: Identifying stress as a multifactorial reaction to perceived adversities, and depression as a manifestation of prolonged stress exposure, our analysis foregrounds the NIIS model. This paradigmatic model reveals the transition from normal stress responses to pathological neuroinflammatory pathways, highlighting neurotransmitter imbalances, neuronal and glial homeostatic disruptions, and ensuing low-grade neuroinflammation as key factors in the pathogenesis of depression under chronic stress conditions. Conclusions: The progression from chronic stress to depression, delineated by the NIIS model, emphasizes the criticality of neuroimmune-inflammatory pathways. This insight not only advances our understanding of their etiopathogenesis but also paves the way for developing precise therapeutic interventions. By offering a detailed framework, the NIIS model serves as a beacon for future explorations and innovative treatments aimed at mitigating the intricate entanglement of stress and depression through a molecular and cellular lens.

The high prevalence of obesity and related nonalcoholic fatty liver disease (NAFLD) necessitates the search for new molecular mechanisms involved in the complex systemic regulation of the development of these diseases. The study of endogenous protective mechanisms in various lipid metabolism disorders is a promising area of science and medicine. Oleoylethanolamide (OEA) is an endogenous lipid mediator that has a multifactorial anorexigenic, anti-inflammatory and hepatoprotective effects due to agonism with PPAR family receptors (PPAR-α, PPAR-γ). This review is aimed at studying PPAR-dependent mechanisms of OEA action in the development of NAFLD. Such aspects as reduction of inflammation and oxidative stress, suppression of hepatocyte apoptosis, reduction of fibrogenesis in the liver and modulation of a wide range of lipid metabolism factors will be discussed in detail.