Atherosclerosis is a chronic cardiovascular disease which increases risk of major cardiovascular events including myocardial infarction and stroke. Elevated plasma concentrations of asymmetric dimethylarginine (ADMA) have long been recognised as a hallmark of cardiovascular disease and are associated with cardiovascular risk factors including hypertension, obesity and hypertriglyceridemia. In this review, we discuss the clinical literature that link ADMA concentrations to increased risk of the development of atherosclerosis. The formation of atherosclerotic lesions relies on the interplay between vascular dysfunction, leading to endothelial activation and the accumulation of inflammatory cells, particularly macrophages, within the vessel wall. Here, we review the mechanisms through which elevated ADMA contributes to endothelial dysfunction, activation and reactive oxygen species (ROS) production; how ADMA may affect vascular smooth muscle phenotype; and finally whether ADMA plays a regulatory role in the inflammatory processes occurring within the vessel wall.

Background: Doxorubicin (DOX) is a potent anti-cancer agent that is widely described in cancer treatment. However, its administration is often limited by its adverse effects, particularly its testicular toxicity, which can induce infertility in male patients. DOX-induced testicular damage is due to oxidative stress, apoptosis, and inflammation. Nanocurcumin (NCR) is a nano-formulated edition of curcumin with a higher therapeutic potential. NCR has demonstrated antioxidant and anti-inflammatory properties. Methods: This study is designed to inspect the potential validity of NCR on DOX-induced testicular damage in male rats. We used thirty-two Wistar albino rats (150–200 g) and divided them into four groups. NCR (80 mg/kg/ dissolved in 1% CMC) was given orally by oral gavage for 14 days. A single dose of DOX (15 mg/kg) (i.p.) was injected on the 7th day of the experiment. Results: DOX treatment reduced the sperm viability and motility rate, cellular antioxidants, and gonadal hormones; it led to higher levels of inflammatory mediators, necrosis, and sloughing in seminiferous tubules. Conversely, NCR treatment significantly alleviated these side effects by improving sperm count/motility and reducing sperm abnormalities. The testicular function recovery was likely driven by stimulating the cytoprotective SIRT1/NF-κB pathway, depressing the testicular level of oxidative indicators such as MDA, TNF-α, iNOS, IL-1β, and NO, and increasing levels of antioxidants such as GSH and SOD. In addition, NCR contradicted the apoptotic changes by downregulating the pro-apoptotic signals Bax and caspase-3, while inducing Bcl-2 upregulation. Moreover, NCR increased levels of gonadal hormones, attenuated histological abnormalities, and preserved testicular structure when compared with the DOX group. Conclusions: NCR treatment can effectively ameliorate DOX-induced testicular toxicity.

Background: Lipid disturbance is a hallmark of cardiometabolic abnormalities and a primary contributor to cardiovascular disease risk. Immunometabolic markers show promise for better risk classification. This study evaluated the uric acid to Platelet ratio (UAPR) as lipid abnormality marker in a broad cohort of Saudi adults. Methods: Data from 7781 adults in the Elta Medical Laboratory database were analysed. Subjects were stratified by lipid status, and UAPR levels were analyzed. Additionally, lipid abnormality distribution across UAPR tertiles and risk profiles, including ROC analysis, were evaluated. Results: UAPR were markedly increased in patients with abnormal lipid profiles while high UAPR (H-UAPR) subjects showed multiple dyslipidemic patterns including elevated levels of triglycerides (TG), low-density lipoprotein (LDL-C), non-high-density lipoprotein (non-HDL-C), and remnant cholesterol (RC), alongside reduced HDL-C levels. Notably, UAPR correlated with all lipid parameters, most strongly and inversely with HDL-C (r = −0.314) and remained independently associated with TG and HDL-C in multivariable regression. Consistently, H-UAPR was common across all dyslipidemic forms, especially low HDL-C, nearly twice as frequent as in N-UAPR (52.4% vs. 35.0%). The odds were specifically increased for low HDL-C (OR = 2.02, p < 0.0001) and a high TC/HDL-C ratio (OR = 2.94, p < 0.0001) in H-UAPR patients. ROC analysis demonstrated that UAPR had moderate yet significant diagnostic performance, particularly for identifying high TC/HDL-C (AUC = 0.671, p < 0.001) and HDL-C (AUC = 0.618, p < 0.001). Conclusions: UAPR shows considerable promise as an immunometabolic marker linked to various dyslipidemic forms with potential for hyperlipidemia screening and stratification, warranting further validation.

Background: The BMI–albumin–neutrophil-to-lymphocyte (BAN) score integrates adiposity, nutritional status, and systemic inflammation, but its role in detecting early cardiometabolic changes remains unclear. This study examined associations of the BAN score with vascular, glycemic, and lipid markers in non-diabetic adults. Methods: This retrospective cross-sectional study included 162 non-diabetic subjects. Associations between the BAN score and vascular, glycemic, and lipid parameters were examined using Spearman’s correlation, ROC analysis, and regression models adjusted for age, sex, smoking status, and medication use. Results: Patients had a median age of 37 years, 72.8% were female, with median BMI 33 kg/m², albumin 4.4 g/dL, and NLR 1.3. Higher BAN scores correlated with systolic blood pressure (SBP) (r = 0.23, p < 0.01), pulse pressure (PP) (r = 0.26, p < 0.001), and HbA1c (r = 0.22, p < 0.01). Compared with the lowest tertile, higher BAN tertiles showed significantly elevated SBP, PP, and HbA1c (p < 0.01). In adjusted models, each one-unit increase in BAN score was associated with higher SBP (β = 1.01, p = 0.037), PP (β = 0.66, p = 0.006), and HbA1c (β = 1.85, p = 0.008). No associations were found with the atherogenic index of plasma (AIP), Castelli risk index I (CRI-I), or Castelli risk index II (CRI-II). ROC analysis showed moderate discriminative ability for hypertension (AUC = 0.66) and HbA1c (AUC = 0.65). Conclusions: The BAN score is associated with a distinctive early cardiometabolic risk, particularly elevated SBP, widened PP, and early glycemic alterations. Further research should define the BAN score’s mechanisms and preventive utility.

Doxorubicin (DOX), a widely used chemotherapeutic, is constrained by its nephrotoxicity, characterized by endothelial injury, inflammation, and oxidative stress. Vascular endothelial growth factor (VEGF) signaling in the kidney serves a dual function. Under normal conditions, it supports the survival of glomerular endothelial cells and maintains vascular stability, but when excessively activated, it disrupts angiogenesis and contributes to kidney injury. In this context, we hypothesize that Nanocurcumin (CUR-NP), a nano-formulated curcumin derivative with enhanced bioavailability, can modulate the VEGF pathway and restore regular renal activity. Thus, this study aims to explore the potential protective effect of CUR-NP on DOX-induced renal injury in male rats. Thirty-two Wistar albino rats were used and distributed into four groups. CUR-NP (80 mg/kg dissolved in 1% CMC) was administered by oral gavage for two weeks. A single dose of DOX (15 mg/kg) (i.p.) was injected on day seven of the study. Results showed that DOX increased the circulating creatinine, urea, and urea-nitrogen levels, while pretreatment with CUR-NP markedly alleviated kidney function. In addition, CUR-NP treatment significantly normalized oxidative stress markers in renal tissues, such as NO, GSH, and SOD, and improved renal pro-inflammatory mediators, TNF-α, IL-6, and NF-κB-p65. DOX caused degeneration of glomeruli and tubules with degenerated epithelial lining and casts in their lumens. Conversely, CUR-NP maintained standard tubular and glomerular structure. Immunohistochemistry showed that DOX strongly upregulated VEGF and AhR, while CUR-NP markedly reduced their expression, countering VEGF/AhR pathway disruption and helping restore physiological signaling.