Matrix metalloproteinases (MMPs) are a family of zinc-dependent endopeptidases that play a crucial role in extracellular matrix (ECM) remodeling and are implicated in the pathogenesis of various cardiovascular diseases (CVDs). Their dysregulation has been linked to atherosclerosis, myocardial infarction (MI), heart failure (HF), and aortic stenosis, contributing to vascular inflammation, plaque destabilization, and adverse cardiac remodeling. Recent research highlights MMPs’ involvement beyond ECM degradation, influencing lipoprotein metabolism, inflammatory signaling, and intracellular processes critical for cardiovascular homeostasis. Despite their pathological role, MMPs remain promising therapeutic targets, with pharmacological inhibitors, gene therapy, and tissue inhibitors of metalloproteinases (TIMPs) emerging as potential interventions. However, the clinical translation of MMP-targeting therapies remains challenging due to off-target effects and complex regulatory mechanisms. This review provides an updated synthesis of the molecular mechanisms, disease-specific roles, and therapeutic implications of MMPs in cardiovascular pathology, aiming to bridge the gap between fundamental research and clinical applications.

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.

Multiple sclerosis (MS) is a chronic autoimmune disorder characterized by inflammation, demyelination, and neurodegeneration within the central nervous system (CNS). While the inflammatory components of MS have been extensively studied, the progressive neurodegenerative aspect remains a critical factor contributing to long-term disability. Therefore, the identification and validation of biomarkers associated with neurodegenerative processes are essential for improved diagnosis, prognosis, and treatment monitoring. This review explores cerebrospinal fluid (CSF) and blood-based biomarkers, including neurofilaments, lipid markers, kynurenines, and other molecular indicators that provide insights into neurodegeneration in MS.

There are numerous articles on the discovery of this arterial polygon, its history being quite long, beginning with the Antiquity and up to the Modern Era. Making an analysis of the primary and secondary sources on this topic, the purpose of this article is to identify the significant moments of the discovery of this arterial polygon, which is an anatomical structure with great importance for neurologists and neurosurgeons. We will present the contributions to this topic from Renaissance and early Modern Era anatomists, such as Andreas Vesalius, Jean Fernel, Gabriel Fallopius, Giulio Cesare Casseri, Adriaan van den Spiegel, Johann Vesling, and Johann Jakob Wepfer von Schaffhausen. We also pointed out that the contribution of the famous British anatomist Sir Thomas Willis (1621–1675) was the most important one. He published De Cerebri Anatome, in 1664, in which he described the vascular arrangement laying at the base of the brain, accompanying it by the exquisite drawings of Christopher Wren. Thus, he demonstrated to the medical world that he had reached the greatest understanding of the structure and function of the circular arterial anastomosis. For this excellent discovery, his followers honored him by giving his name to this arterial circle.

Diabetic retinopathy (DR), a leading cause of vision impairment worldwide, is characterized by progressive damage to the retina due to prolonged hyperglycemia. Despite advances in treatment, current interventions largely target late-stage vascular complications, leaving underlying neurodegenerative processes insufficiently addressed. This article explores the crucial role in neuronal survival, axonal growth, and synaptic plasticity and the neuroprotective potential of Brain-Derived Neurotrophic Factor (BDNF) as a therapeutic strategy for enhancing retinal resilience in DR. Furthermore, it discusses innovative delivery methods for BDNF, such as gene therapy and nanocarriers, which may overcome the challenges of achieving sustained and targeted therapeutic levels in the retina, focusing on early intervention to preserve retinal function and prevent vision loss.