Several chronic liver diseases are characterized by a clear gender disparity. Among them, hepatocellular carcinoma (HCC) shows significantly higher incidence rates in men than in women. The different epidemiological distribution of risk factors for liver disease and HCC only partially accounts for these gender differences. In fact, the liver is an organ with recognized sexual dysmorphism and is extremely sensitive to the action of androgens and estrogens. Sex hormones act by modulating the risk of developing HCC and influencing its aggressiveness, response to treatments, and prognosis. Furthermore, androgens and estrogens are able to modulate the action of other factors and cofactors of liver damage (e.g., chronic HBV infection, obesity), significantly influencing their carcinogenic power. The purpose of this review is to examine the factors related to the different gender distribution in the incidence of HCC as well as the pathophysiological mechanisms involved, with particular reference to the central role played by sex hormones.

Hepatitis B virus (HBV) is a major cause of chronic hepatitis, liver cirrhosis, and hepatocellular carcinoma. Despite the advent of vaccines and potent antiviral agents able to suppress viral replication, recovery from chronic HBV infection is still an extremely difficult goal to achieve. Complex interactions between virus and host are responsible for HBV persistence and the risk of oncogenesis. Through multiple pathways, HBV is able to silence both innate and adaptive immunological responses and become out of control. Furthermore, the integration of the viral genome into that of the host and the production of covalently closed circular DNA (cccDNA) represent reservoirs of viral persistence and account for the difficult eradication of the infection. An adequate knowledge of the virus–host interaction mechanisms responsible for viral persistence and the risk of hepatocarcinogenesis is necessary for the development of functional cures for chronic HBV infection. The purpose of this review is, therefore, to analyze how interactions between HBV and host concur in the mechanisms of infection, persistence, and oncogenesis and what are the implications and the therapeutic perspectives that follow.

Although mast cells have long been known, they are not yet fully understood. They are traditionally recognized for their role in allergic reactions through the IgE/FcεRI axis, but different groups of surface receptors have since been characterized, which appear to be involved in the manifestation of peculiar clinical features. In particular, MRGPRX2 has emerged as a crucial receptor involved in degranulating human skin mast cells. Because of mast cells’ close proximity to peripheral nerve endings, it may play a key role in neuroimmune interactions. This paper provides an overview of mast cell contributions to hypersensitivity and so-called “pseudoallergic” reactions, as well as an update on neuroinflammatory implications in the main models of airway and skin allergic diseases. In particular, the main cellular characteristics and the most relevant surface receptors involved in MC pathophysiology have been reappraised in light of recent advancements in MC research. Molecular and clinical aspects related to MC degranulation induced by IgE or MRGPRX2 have been analyzed and compared, along with their possible repercussions and limitations on future therapeutic perspectives.

Hypercholesterolemia plays a crucial role in the formation of lipid plaques, particularly with elevated low-density lipoprotein (LDL-C) levels, which are linked to increased risks of cardiovascular disease, cerebrovascular disease, and peripheral arterial disease. Controlling blood cholesterol values, specifically reducing LDL-C, is widely recognized as a key modifiable risk factor for decreasing the morbidity and mortality associated with cardiovascular diseases. Historically, statins, by inhibiting the enzyme β-hydroxy β-methylglutaryl-coenzyme A (HMG)-CoA reductase, have been among the most effective drugs. However, newer non-statin agents have since been introduced into hypercholesterolemia therapy, providing a viable alternative with a favorable cost–benefit ratio. This paper aims to delve into the latest therapies, shedding light on their mechanisms of action and therapeutic benefits.

Celiac disease (CeD) is a chronic, lifelong, multifactorial, polygenic, and autoimmune disorder, characteristically triggered by exposure to the exogenous factor “gluten” in genetically predisposed individuals, with resulting duodenal inflammation and enteropathy, as well as heterogeneous multisystemic and extraintestinal manifestations. The immunopathogenesis of CeD is complex, favored by a peculiar human leukocyte antigen (HLA) genetic predisposition, leading to gluten presentation by antigen-presenting cells to CD4+ T helper (Th) cells, T cell–B cell interactions, and production of specific antibodies, resulting in the immune-mediated killing of enterocytes and, macroscopically, in duodenal inflammation. Here, the most relevant correlations between cellular and molecular aspects and clinical manifestations of this complex disease are reviewed, with final considerations on nutritional aspects for disease management.

The aim was to assess the impact of glucagon-like peptide-1 receptor agonists (GLP-1 RA) treatment on the progression of ascending aorta dilatation in patients with type 2 diabetes mellitus (T2DM). A total of 127 T2DM patients with subclinical ascending aortic dilatation (35–45 mm) were prospectively enrolled. Fifty-seven initiated GLP-1 RA therapy (liraglutide, semaglutide, or dulaglutide), while 70 continued on standard care. Ascending aortic diameter was measured by computed tomography angiography (CTA) at baseline and 24 months, alongside circulating markers of vascular remodeling: matrix metalloproteinase-9 (MMP-9), tissue inhibitor of metalloproteinases-1 (TIMP-1), C-reactive protein (CRP), and osteoprotegerin (OPG). Progression of aortic dilatation was significantly lower in the GLP-1 RA group compared with controls (+0.36 ± 0.20 mm vs. +1.05 ± 0.28 mm; p < 0.001). Therapy correlated with decreased MMP-9 and CRP (p < 0.01) and increased TIMP-1 and OPG (p < 0.05). The use of GLP-1 RA was an independent predictor of low progression, even in multivariate models after adjusting for demographic, metabolic, and biomarker data. GLP-1 RA therapy was associated with reduced progression of ascending aortic dilatation in T2DM, supporting a potential vasoprotective role beyond glucose lowering.