Type 2 diabetes mellitus (T2DM) remains one of the most problematic and economic consumer disorders worldwide, with growing prevalence and incidence. Over the last years, substantial research has highlighted the intricate relationship among gut microbiota, dysbiosis and metabolic syndromes development. Changes in the gut microbiome composition lead to an imbalanced gastrointestinal habitat which promotes abnormal production of metabolites, inflammatory status, glucose metabolism alteration and even insulin resistance (IR). Short-chain fatty acids (SCFAs), trimethylamine N-oxide (TMAO), lipopolysaccharide, aromatic amino acids and their affiliated metabolites, contribute to T2DM via different metabolic and immunologic pathways. In this narrative review, we discuss the immunopathogenic mechanism behind gut dysbiosis, T2DM development and the major known diabetic microvascular complications (retinopathy, neuropathy and nephropathy), the beneficial use of pre- and pro-biotics and fecal microbiota transplantation in T2DM management and new findings and future perspectives in this field.

We are witnessing the globalization of a specific type of arteriosclerosis with rising prevalence, incidence and an overall cardiovascular disease burden. Currently, atherosclerosis increasingly affects the younger generation as compared to previous decades. While early preventive medicine has seen improvements, research advances in laboratory and clinical investigation promise to provide us with novel diagnosis tools. Given the physio-pathological complexity and epigenetic patterns of atherosclerosis and the discovery of new molecules involved, the therapeutic field of atherosclerosis has room for substantial growth. Thus, the scientific community is currently investigating the role of nucleotide-binding and oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome, a crucial component of the innate immune system in different inflammatory disorders. NLRP3 is activated by distinct factors and numerous cellular and molecular events which trigger NLRP3 inflammasome assembly with subsequent cleavage of pro-interleukin (IL)-1β and pro-IL-18 pathways via caspase-1 activation, eliciting endothelial dysfunction, promotion of oxidative stress and the inflammation process of atherosclerosis. In this review, we introduce the basic cellular and molecular mechanisms of NLRP3 inflammasome activation and its role in atherosclerosis. We also emphasize its promising therapeutic pharmaceutical potential.

Type 2 diabetes mellitus (T2DM) still holds the title as one of the most debilitating chronic diseases with rising prevalence and incidence, including its complications such as retinal, renal, and peripheral nerve disease. In order to develop novel molecules for diagnosis and treatment, a deep understanding of the complex molecular pathways is imperative. Currently, the existing agents for T2DM treatment target only blood glucose levels. Over the past decades, specific building blocks of proteins—branched-chain amino acids (BCAAs) including leucine, isoleucine, and valine—have gained attention because they are linked with insulin resistance, pre-diabetes, and diabetes development. In this review, we discuss the hypothetical link between BCAA metabolism, insulin resistance, T2DM, and its microvascular complications including diabetic retinopathy and diabetic nephropathy. Further research on these amino acids and their derivates may eventually pave the way to novel biomarkers or therapeutic concepts for the treatment of diabetes and its accompanied complications.

Calcific aortic valve disease (CAVD) is a major cause of cardiovascular mortality and morbidity, with increased prevalence and incidence. The underlying mechanisms behind CAVD are complex, and are mainly illustrated by inflammation, mechanical stress (which induces prolonged aortic valve endothelial dysfunction), increased oxidative stress (OS) (which trigger fibrosis), and calcification of valve leaflets. To date, besides aortic valve replacement, there are no specific pharmacological treatments for CAVD. In this review, we describe the mechanisms behind aortic valvular disease, the involvement of OS as a fundamental element in disease progression with predilection in AS, and its two most frequent etiologies (calcific aortic valve disease and bicuspid aortic valve); moreover, we highlight the potential of OS as a future therapeutic target.

Mesenchymal stem cells (MSCs) have emerged as a relevant strategy in regenerative medicine due to their multipotent differentiation capacity, immunomodulatory properties, and therapeutic applications in various medical fields. This review explores the therapeutic use of MSCs, focusing on their role in treating autoimmune disorders and neoplastic diseases and in tissue regeneration. We discuss the mechanisms underlying MSC-mediated tissue repair, including their paracrine activity, migration to injury sites, and interaction with the immune system. Advances in cellular therapies such as genome engineering and MSC-derived exosome treatments further enhance their applicability. Key methodologies analyzed include genomic studies, next-generation sequencing (NGS), and bioinformatics approaches to optimize MSC-based interventions. Additionally, we reviewed preclinical and clinical evidence demonstrating the therapeutic potential of MSCs in conditions such as graft-versus-host disease, osteoarthritis, liver cirrhosis, and neurodegenerative disorders. While promising, challenges remain regarding standardization, long-term safety, and potential tumorigenic risks associated with MSC therapy. Future research should focus on refining MSC-based treatments to enhance efficacy and minimize risks. This review underscores the need for large-scale clinical trials to validate MSC-based interventions and fully harness their therapeutic potential.

At the end of 2019, a variation of a coronavirus, named SARS-CoV-2, has been identified as being responsible for a respiratory illness disease (COVID-19). Since ventilation is an important factor that influences airborne transmission, we proposed to study the impact of heating, ventilation and air-conditioning (HVAC) with a variable air volume (VAV) primary air system, on the dispersion of infectious aerosols, in a cardiac intensive care unit, using a transient simulation with computational fluid dynamics (CFD), based on the finite element method (FEM). We analyzed three scenarios that followed the dispersion of pathogen carrying expiratory droplets particles from coughing, from patients possibly infected with COVID-19, depending on the location of the patients in the intensive care unit. Our study provides the mechanism for spread of infectious aerosols, and possibly of COVID-19 infection, by air conditioning systems and also highlights important recommendations for disease control and optimization of ventilation in intensive care units, by increasing the use of outdoor air and the rate of air change, decreasing the recirculation of air and using high-efficiency particulate air (HEPA) filters. The CFD-FEM simulation approach that was applied in our study could also be extended to other targets, such as public transport, theaters, philharmonics and amphitheaters from educational units.