Over the past decades, obesity has become a rising health problem as the accessibility to high calorie, low nutritional value food has increased. Research shows that some bioactive components in fruits and vegetables, such as carotenoids, could contribute to the prevention and treatment of obesity. Some of these carotenoids are responsible for vitamin A production, a hormone-like vitamin with pleiotropic effects in mammals. Among these effects, vitamin A is a potent regulator of adipose tissue development, and is therefore important for obesity. This review focuses on the role of the provitamin A carotenoid β-carotene in human health, emphasizing the mechanisms by which this compound and its derivatives regulate adipocyte biology. It also discusses the physiological relevance of carotenoid accumulation, the implication of the carotenoid-cleaving enzymes, and the technical difficulties and considerations researchers must take when working with these bioactive molecules. Thanks to the broad spectrum of functions carotenoids have in modern nutrition and health, it is necessary to understand their benefits regarding to metabolic diseases such as obesity in order to evaluate their applicability to the medical and pharmaceutical fields.

Finasteride is commonly prescribed to treat benign prostate hyperplasia and male-pattern baldness in cis men and, more recently, trans individuals. However, the effect of finasteride on cardiovascular disease remains elusive. We evaluated the role of finasteride on atherosclerosis using low-density lipoprotein (LDL) receptor-deficient (Ldlr^-/-) mice. Next, we examined the relevance to humans by analyzing the data deposited between 2009 and 2016 in the National Health and Nutrition Examination Survey. We show that finasteride reduces total plasma cholesterol and delays the development of atherosclerosis in Ldlr^-/- mice. Finasteride reduced monocytosis, monocyte recruitment to the lesion, macrophage lesion content, and necrotic core area, the latter of which is an indicator of plaque vulnerability in humans. RNA sequencing analysis revealed a downregulation of inflammatory pathways and an upregulation of bile acid metabolism, oxidative phosphorylation, and cholesterol pathways in the liver of mice taking finasteride. Men reporting the use of finasteride showed lower plasma levels of cholesterol and LDL-cholesterol than those not taking the drug. Our data unveil finasteride as a potential treatment to delay cardiovascular disease in people by improving the plasma lipid profile.

Aims: To investigate how psychosocial stress contributes to accelerated thrombosis, focusing on platelet activation and hyperreactivity. The specific objective was to identify novel platelet regulators involved in stress-mediated thrombosis, with a particular emphasis on the tetraspanin CD37. Methods and results: To explore how stress contributes to platelet hyperreactivity, platelets were isolated from (i) mice that experienced chronic variable stress and stress-free controls (n = 8/group) and (ii) human subjects with self-reported high- and no-stress levels (n = 18/group), followed by RNA-sequencing. By comparing mutually expressed transcripts, a subset of genes differentially expressed following psychosocial stress was identified in both human and mouse platelets. In both mice and humans, platelet CD37 positively associates with platelet aggregation responses that underlie thrombosis, with Cd37−/− platelets exhibiting impaired integrin αIIbβ3 signalling, characterized by reduced platelet fibrinogen spreading and decreased agonist-induced αIIbβ3 activation. Consistent with a role for CD37 in regulating platelet activation responses, chimeric mice that received Cd37−/− bone marrow experienced a significantly increased time to vessel occlusion in the carotid artery FeCl3 model compared to mice reconstituted with wild-type bone marrow. CD37 deficiency did not alter haemostasis, as platelet count, coagulation metrics, prothrombin time, and partial thromboplastin time did not differ in Cd37−/− mice relative to wild-type mice. Consistent with this, bleeding time did not differ between wild-type and Cd37−/− mice following tail tip transection. Conclusion: This study provides new insights into the platelet-associated mechanisms underlying stress-mediated thrombosis. Identifying CD37 as a novel regulator of platelet activation responses offers potential therapeutic targets for reducing the thrombotic risk associated with psychosocial stress. The findings also contribute to understanding how psychosocial stress accelerates thrombotic events and underscore the importance of platelet activation in this process. Clinical trial registration: NCT02106429, NCT03022552

BACKGROUND: People with HIV are at higher risk of atherosclerotic cardiovascular disease than uninfected individuals; however, the molecular mechanisms behind this association remain elusive due to the lack of suitable animal models. METHODS: To study the impact of HIV on atherosclerotic cardiovascular disease, we infected the atheroprone Ldlr ^−/− mice with the chimeric virus EcoHIV. RESULTS: In comparison to uninfected controls, EcoHIV infection increased the ratio of circulating inflammatory monocytes, monocyte recruitment, and CD68 ⁺ content in the atherosclerotic lesion. These changes occurred independently of alterations in plasma lipid profile or lesion size between groups. Lesions of EcoHIV-infected mice displayed greater vulnerability to rupture, as determined by increased necrotic core area and CD38 ⁺ content, and reduced presence of collagen compared with uninfected mice. Last, we report the presence of active viral replication of EcoHIV in the atherosclerotic lesion. CONCLUSIONS: Our data suggest that EcoHIV infection in Ldlr ^−/− mice resembles the pathogenesis of atherosclerotic cardiovascular disease in people with HIV. Our findings have therapeutic implications for people with HIV, a vulnerable population with an elevated risk of cardiovascular disease.