Adrian Chabowski

Psoriasis is a chronic, immune-mediated inflammatory disease affecting the skin, nails, and joints. Its complex pathogenesis results from interactions between genetic susceptibility and environmental factors and is accompanied by an increased risk of multiple systemic comorbidities, particularly cardiovascular disease. Growing evidence indicates that both conditions share common molecular pathways driven by chronic inflammation, endothelial dysfunction, metabolic disturbances, and immune dysregulation. Among the emerging molecular biomarkers, chemerin, endocan, and growth differentiation factor-15 (GDF-15) have attracted considerable attention due to their role in vascular homeostasis, adipose tissue biology, glucose metabolism, and inflammatory signaling. This review summarizes current evidence on the involvement of these biomarkers in psoriasis and cardiovascular disease, highlighting their contribution to the molecular mechanisms underlying the psoriasis–cardiovascular disease axis. Furthermore, we discussed their potential usefulness as candidate biomarkers for cardiovascular risk. However, prospective validation is strictly required to confirm their clinical utility and establish their incremental predictive value beyond conventional risk factors.

Adipose-derived mesenchymal stem cells (ADMSCs) are a crucial source of new adipocytes and play a significant role in regulating adipose tissue physiology. Interestingly, mature adipocytes differentiated from the ADMSCs maintain some characteristic features of their respective depots as well as the metabolic status of the donor patients. The above is true with respect to the cells’ secretory profile and their glycerolipid and sphingolipid composition. In the current paper, we focused our attention on the phospholipid profile of the adipocytes derived from ADMSCs, with a particular emphasis placed on how obesity and metabolic syndrome affect their composition. Surprisingly, the cells displayed a significantly greater (even up to 10-fold) overall phospholipid concentration when compared with the primary human adipocytes described in the literature. The phenomenon may be explained by a geometrical property known as surface-to-volume ratio, which dictates that the total surface area of many small cells (our adipocytes) is greater than the total area of less numerous but more voluminous cells in vivo. Interestingly, also a donor’s metabolic status can influence the characteristics of these fat cells. The study found that subcutaneous adipocytes, when derived from patients with obesity and metabolic syndrome, had an increased concentration of phosphatidylcholine (PC), phosphatidylethanolamine (PE), phosphatidylinositol (PI), and sphingomyelin (SM). The above-mentioned changes often reflect the ones found in vivo and may well be the early metabolic disarrangements that occur in the progress of obesity.

Background: Lipoproteins are molecules composed of phospholipids and apolipoproteins that transport triacylglycerol and cholesterol in blood and are implicated in the development of many diseases. Methods: In this study, we fill a knowledge gap by precisely characterizing the apolipoprotein profile (with Bio-Plex Human Apolipoprotein Assay) in three metabolically separate groups of individuals (lean individuals and obese individuals without and with metabolic syndrome) and at four distinct time points (0, 3, 6, and 12 months post bariatric surgery). Results: Obese patients had a higher baseline ApoB/ApoA1 ratio, which returned to the reference level over the follow-up period. The above is of clinical importance, as the ratio is a predictor of adverse cardiovascular events common in obese subjects. Interestingly, plasma concentrations of most of the investigated apolipoproteins appeared to be relatively stable at the onset of the experiment, with changes observed later in time. We detected significant drops in the levels of ApoC3, ApoD, and ApoH that occurred as early as three months post intervention. On the other hand, the levels of ApoA2, ApoE, and ApoJ increased with time. Of the above, ApoE is known to be involved in the removal of TAGs and cholesterol from the blood. Conversely, ApoJ appears to be one of the determinants of the tissues’ responsiveness to insulin. Thus, it may be an indicator of the reduced insulin resistance observed a few months after the surgery. Conclusions: Overall, the investigated proteins have a documented role in the development and progression of vascular pathologies. Hence, our results may be interpreted as a sign of improved cardiovascular fitness of our patients.

Aerobic exercise training (AET) and numerous dietary interventions, including nitrate and resveratrol supplementation, display overlapping mechanisms affecting mitochondrial bioenergetics and metabolism in diverse tissues. However, it remains unclear if a combination of these interventions results in additive benefits for the prevention of obesity-related co-morbidities. To investigate this, C57Bl/6N mice consumed a high-fat diet and remained sedentary (HFD) or performed AET for 6 weeks in the absence (HFD+AET) or presence of nitrate+resveratrol supplementation (HFD+AET+NR). As expected, AET attenuated body weight gain, reduced adipocyte cross-sectional area and markers of cellular stress/inflammation within white adipose tissue, and increased mitochondrial respiratory capacity and decreased lipid content within skeletal muscle independent of supplementation. While AET alone was sufficient to improve glucose tolerance, the addition of +NR provided modest liver-specific enhancements including increased mitochondrial respiratory capacity, reduced reactive lipid accumulation, and a unique proteomic signature associated with altered amino acid metabolism, corresponding to further reductions in systemic fasting blood glucose levels. These data suggest that while AET remains a primary lifestyle intervention to drive metabolic improvements during high-fat feeding, targeted dietary supplementation may provide tissue-specific enhancements, particularly within the liver, that complement exercise adaptations.

Background: Kidney disorders are strongly related to metabolic disturbances, including obesity and type 2 diabetes. Excessive intake of sugar and saturated fats promotes lipid accumulation, cellular energy issues and inflammatory responses. Cannabigerol (CBG), a non-psychotropic phytocannabinoid, has recently gained attention for its metabolic, anti-inflammatory and potential protective properties. Methods: The present study investigated the effect of two weeks of CBG administration (last 14 days of the experiment) on fatty acid (FA) composition, FA metabolic pathways and FA transporters in rats subjected to a high-fat high-sucrose diet (HFHS) for 6 weeks. Male Wistar rats were divided into four groups: Control, CBG, HFHS, and HFHS+CBG. Kidney tissue and urine samples were analyzed by gas–liquid chromatography (GLC) for lipid fractions and FA profiles, while protein expression of FA transporters and metabolic enzymes was assessed by immunoblotting. Polysaccharides and collagen fibers were visualized using Periodic Acid-Schiff (PAS) and AZAN staining, respectively. ELISA and colorimetric kits were used to measure urinary albumin and creatinine contents. Results: HFHS feeding altered renal lipid homeostasis, increasing saturated and monounsaturated fatty acids (SFA and MUFA, respectively) levels and affecting desaturation and elongation ratios. CBG supplementation affected renal lipid metabolism by lowering triacylglycerol (TAG) accumulation, restoring polyunsaturated fatty acids (PUFA) in phospholipid (PL) and altering FA ratios, suggesting an improvement in lipid balance. CBG also increased the expression of carnitine palmitoyltransferase 1 (CPT1) and lipoprotein lipase (LPL) and decreased the expression of stearoyl-CoA desaturase 1 (SCD1) and fatty acid synthase (FAS), suggesting a shift toward enhanced FA oxidation and reduced lipogenesis. Conclusions: Overall, CBG exerted good effects on renal lipid metabolism and may mitigate early lipid-mediated injury associated with metabolic kidney disorders.

Skin diseases frequently coexist with other disorders, such as metabolic syndrome, diabetes mellitus, depression, psoriatic arthritis, and cardiovascular disease. Altered levels of distinct chemokines, like CCL5/RANTES, CXCL12/SDF-1a, CCL7/MCP-3, CCL2/MCP-1, CXCL1/GROa, and the eotaxin family, contribute to the development and/or exacerbation of inflammation, which is a common feature of numerous skin diseases as well as metabolic syndrome. The pathological and molecular connections between chronic inflammatory skin diseases and metabolic syndrome are increasingly recognized as being driven by shared inflammatory pathways, oxidative stress, and adipokine dysregulation. While systemic inflammation acts as a common thread, the precise mechanisms for some conditions remain partially understood. Nevertheless, the exact pathological and molecular connections between skin diseases (i.e., psoriasis, atopic dermatitis, pemphigus vulgaris, acute and chronic spontaneous urticaria, bullous pemphigoid, squamous cell carcinoma, alopecia areata, systemic sclerosis, discoid lupus erythematosus, diffuse large B-cell lymphoma) and metabolic syndrome are not yet fully understood. This narrative review summarizes the robust association between various chronic inflammatory skin diseases and metabolic syndrome in the context of pro-inflammatory chemokines.

Background: This study investigated the effects of cannabidiol (CBD) on early-stage inflammation, a key factor in the progression of liver diseases from metabolic dysfunction-associated steatotic liver disease (MASLD) to metabolic dysfunction-associated steatohepatitis (MASH) and irreversible cirrhosis. The study focused on CBD’s influence on the pro-inflammatory n-6 and anti-inflammatory n-3 pathways, on arachidonic acid (AA) levels as an early marker of inflammation, and the expression of enzymes involved in AA metabolism, as well as inflammatory cytokines and chemokines. Methods: Forty male Wistar rats were randomly divided into four groups: control (C)—fed a standard diet and treated with cannabidiol vehicle for the last 14 days, control + cannabidiol (C + CBD) – fed a standard diet and treated with CBD for the last 14 days, high-fat diet (HFD) – fed a high-fat diet and treated with cannabidiol vehicle for the last 14 days, high-fat diet + cannabidiol (HFD + CBD)—fed a high-fat diet and treated with cannabidiol for the last 14 days. At the end of the treatment period, all the rats were fasted for 24 h, anesthetized, and sacrificed. Gas–liquid chromatography was used to measure n-6 and n-3 pathway polyunsaturated fatty acids (PUFAs) activities and AA levels in lipid fractions in the liver. The Multiplex immunoassay assessed cytokine and chemokine content in liver tissue, while Western Blot analyzed the expression of selected enzymes. Results: Initial findings indicated CBD’s potential in reducing inflammation and its therapeutic efficacy in preventing MASH development induced by HFD. The results indicated that supplementing with CBD led to a decrease in the n-6 PUFA pathway, known for its pro-inflammatory effects, and an increase in the anti-inflammatory n-3 PUFA pathway. These changes were simultaneous with lower levels of arachidonic acid, which is crucial for the formation of inflammatory mediators. CBD influenced the expression of enzymes like COX-1 and COX-2 involved in AA metabolism and reduced the levels of pro-inflammatory cytokines. Conclusions: Our observations confirmed that CBD, which affects early indicators of inflammation, has the potential to become a new and safe, promising supportive drug for hepatic inflammation and steatosis treatment. Graphical

Psoriasis is a chronic, inflammatory skin disease occurring worldwide that significantly affects patients’ quality of life. This common skin condition is characterized by abnormal hyperplasia of keratinocytes, which leads to the formation of raised, scaly plaques, typically located on the head, elbows, knees, and lumbar region. Psoriasis usually requires long-term drug therapy, which aims not only to combat skin symptoms but also to improve quality of life. Although topical treatments, systemic treatments (methotrexate, cyclosporine, acitretin), and phototherapy play a role, biologic agents have improved the efficacy of treatment of moderate-to-severe psoriasis. The purpose of this article is to comprehensively review the clinical trial data and evaluate and compare the key features of the currently approved biologic drugs for the treatment of psoriasis.

Psoriasis is a chronic, immune-mediated inflammatory disease that affects the skin, nails, joints, and cardiovascular system. In this study, involving 50 psoriatic patients and 28 healthy controls (patients with inguinal hernia), serum elafin levels were measured using enzyme-linked immunosorbent assay (ELISA). The results revealed significantly higher serum elafin levels in the psoriatic group compared to healthy individuals. Moreover, we observed a statistically significant positive correlation between serum elafin levels and the Psoriasis Area and Severity Index (PASI) scores. These findings indicate that elafin—a protein involved in psoriasis pathogenesis—is significantly altered in the serum of psoriatic patients and may be associated with disease severity.