In recent decades, as a result of rising mortality rates due to cardiovascular diseases (CVDs), there has been a growing urgency to find alternative approaches to conventional pharmaceutical treatment to prevent the onset of chronic diseases. Arthrospira platensis, commonly known as Spirulina, is a blue-green cyanobacterium, classified as a “superfood”, used worldwide as a nutraceutical food supplement due to its remarkable nutritional value, lack of toxicity, and therapeutic effects. Several scientific studies have evaluated the cardioprotective role of Spirulina. This article presents a comprehensive review of the therapeutic benefits of Spirulina in improving cardio- and cerebrovascular health. It focuses on the latest experimental and clinical findings to evaluate its antihypertensive, antidiabetic, and antihyperlipidemic properties. The objective is to highlight its potential in preventing and managing risk factors associated with cardiovascular disease (CVD).

Cardiometabolic diseases, including cardiovascular disorders and type 2 diabetes mellitus, are the leading cause of morbidity and mortality worldwide, placing a significant burden on healthcare systems. Although advances in imaging and risk stratification have improved disease management, conventional diagnostic and prognostic tools often lack the requisite sensitivity and specificity for early and precise risk stratification. This limitation stems from their poor ability to capture the full molecular complexity of these conditions, underscoring an urgent need for innovative biomarkers to bridge these gaps. MicroRNAs, small non-coding RNAs that regulate gene expression post-transcriptionally, have emerged as promising candidates. Their characteristics offer several advantages over traditional methods, including exceptional stability in biological fluids, strong tissue and disease specificity, and the ability to reflect dynamic pathological changes. These unique features enable miRNAs to detect subtle molecular alterations that may precede clinical symptoms, thereby overcoming key limitations of current diagnostic approaches. Altered circulating miRNA profiles have been linked to pathological processes such as endothelial dysfunction, inflammation, oxidative stress, and maladaptive cardiac remodeling. This review provides a comprehensive overview of the current evidence supporting the diagnostic and prognostic role of circulating miRNAs in cardiometabolic disease. We highlight their potential as early detection biomarkers, tools for patient stratification, and indicators of therapeutic response. Furthermore, we discuss key limitations to clinical translation, including methodological variability, challenges in sample handling, differences in normalization strategies, and platform-dependent quantification inconsistencies. Overcoming these obstacles and achieving robust large-scale clinical validation will be essential to fully harness the potential of miRNAs as next-generation molecular signatures in precision medicine.

High glucose–induced endothelial dysfunction is an important pathological feature of diabetic vasculopathy. While genome-wide studies have identified an association between type 2 diabetes mellitus (T2DM) and increased expression of a C2 calcium-dependent domain containing 4B (C2CD4B), no study has yet explored the possible direct effect of C2CD4B on vascular function. Vascular reactivity studies were conducted using a pressure myograph, and nitric oxide and oxidative stress were assessed through difluorofluorescein diacetate and dihydroethidium, respectively. We demonstrate that high glucose upregulated both mRNA and protein expression of C2CD4B in mice mesenteric arteries in a time-dependent manner. Notably, the inhibition of C2CD4B expression by genetic knockdown efficiently prevented hyperglycemia–induced oxidative stress, endothelial dysfunction, and loss of nitric oxide (NO) bioavailability. Recombinant C2CD4B evoked endothelial dysfunction of mice mesenteric arteries, an effect associated with increased reactive oxygen species (ROS) and decreased NO production. In isolated human umbilical vein endothelial cells (HUVECs), C2CD4B increased phosphorylation of endothelial nitric oxide synthase (eNOS) at the inhibitory site Thr495 and reduced eNOS dimerization. Pharmacological inhibitors of phosphoinositide 3-kinase (PI3K), Akt, and PKCα effectively attenuated oxidative stress, NO reduction, impairment of endothelial function, and eNOS uncoupling induced by C2CD4B. These data demonstrate, for the first time, that C2CD4B exerts a direct effect on vascular endothelium via a phosphoinositide 3-kinase (PI3K)/Akt/PKCα–signaling pathway, providing a new perspective on C2CD4B as a promising therapeutic target for the prevention of oxidative stress in diabetes–induced endothelial dysfunction.

A detailed review on sensing strategies for the recognition of emerging and standard biomarkers for the early diagnosis and prognosis of cardiovascular diseases, including their potential integration into point-of-care biosensor platforms.