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Abstract: Cardiovascular disease remains a leading cause of mortality despite major advances in lipid lowering and risk-factor control, highlighting the importance of residual cardiovascular risk. Inflammation is a central driver of atherosclerosis, while obesity promotes chronic low-grade inflammation, adipose tissue dysfunction, ectopic fat accumulation, and vascular injury. This narrative review focuses on obesity-associated inflammation as an upstream contributor to residual atherosclerotic risk and evaluates whether incretin-based therapies modify this pathway through weight loss, metabolic improvement, and additional inflammatory or vascular mechanisms. Data from mechanistic studies, biomarker analyses, vascular imaging studies, and cardiovascular outcome trials are reviewed. Anti-inflammatory trials support inflammation as a modifiable therapeutic pathway, although clinical benefit depends on the therapeutic target, timing, and patient selection. Glucagon-like peptide-1 receptor agonists reduce inflammatory and oxidative stress biomarkers and show anti-atherosclerotic effects in experimental models, but human vascular imaging data remain inconclusive. Cardiovascular outcome trials establish benefit with several GLP-1 receptor agonists, including semaglutide in selected patients with overweight or obesity without diabetes. However, direct human evidence for receptor-mediated anti-inflammatory or anti-atherosclerotic effects remains limited, and the relative contributions of weight loss, metabolic improvement, and additional mechanisms remain uncertain.
Keywords: atherosclerosis, inflammation, residual inflammatory risk, obesity, glucagon-like peptide-1 receptor agonists, semaglutide, tirzepatide, incretin-based therapy, cardiovascular prevention, adipose tissue inflammation
Published in DiRROS: 07.09.2026; Views: 123; Downloads: 80
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Abstract: Oxidative stress and neuroinflammation are important processes involved in Alzheimer’s disease (AD) and mild cognitive impairment (MCI). Numerous risk factors, including genetic background, can affect the complex interplay between those mechanisms in the aging brain and can also affect typical AD hallmarks: amyloid plaques and neurofibrillary tangles. Our aim was to evaluate the association of polymorphisms in oxidative stress- and inflammation-related genes with cerebrospinal fluid (CSF) biomarker levels and cognitive test results. The study included 54 AD patients, 14 MCI patients with pathological CSF biomarker levels, 20 MCI patients with normal CSF biomarker levels and 62 controls. Carriers of two polymorphic IL1B rs16944 alleles had higher CSF Aβ1–42 levels (p = 0.025), while carriers of at least one polymorphic NFE2L2 rs35652124 allele had lower CSF Aβ1–42 levels (p = 0.040). Association with IL1B rs16944 remained significant in the AD group (p = 0.029). Additionally, MIR146A rs2910164 was associated with Aβ42/40 ratio (p = 0.043) in AD. Significant associations with cognitive test scores were observed for CAT rs1001179 (p = 0.022), GSTP1 rs1138272 (p = 0.005), KEAP1 rs1048290 and rs9676881 (both p = 0.019), as well as NFE2L2 rs35652124 (p = 0.030). In the AD group, IL1B rs1071676 (p = 0.004), KEAP1 rs1048290 and rs9676881 (both p = 0.035) remained associated with cognitive scores. Polymorphisms in antioxidative and inflammation genes might be associated with CSF biomarkers and cognitive test scores and could serve as additional biomarkers contributing to early diagnosis of dementia.
Keywords: Alzheimer’s disease, oxidative stress, inflammation
Published in DiRROS: 03.08.2026; Views: 275; Downloads: 139
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Abstract: Oncological patients make up a large proportion of all surgical patients. Through its influence on the patient’s inflammatory and immune system, the choice of anaesthetic technique has an indirect impact on the health of the individual patient and on public health. Both the specific and the non-specific immune system have a major influence on the recurrence of carcinomas. The pathophysiological basis for growth and metastasis after surgery is the physiological response to stress. Inflammation is the organism’s universal response to stress. Anaesthetics and adjuvants influence perioperative inflammation in different ways and have an indirect effect on tumour growth and metastasis. In vitro studies have shown how individual anaesthetics influence the growth and spread of cancer, but clinical studies have not confirmed these results. Nevertheless, it is advisable to use an anaesthetic that has shown lesser effect on the growth of cancer cells in vitro. Conclusions In this review, we focus on the area of the effects of anaesthesia on tumour growth. The field is still relatively unexplored, there are only few clinical prospective studies and their results are controversial. Based on the review of new research findings we report on recommendations about anaesthetics and anaesthetic techniques that might be preferable for oncological surgical procedures.
Keywords: cancer growth, anaestesia, inflammation
Published in DiRROS: 24.06.2026; Views: 289; Downloads: 99
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Keywords: paraoxonase 1, cardiopulmonary bypass, oxidative stress, inflammation, glucocorticoids, methylprednisolone
Published in DiRROS: 11.06.2026; Views: 310; Downloads: 296
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Abstract: Despite progress in treatment, elevated levels of low-density lipoprotein cholesterol (LDL-C) and lipoprotein (a) (Lp(a)), represent a significant part of the residual risk. Both are associated with inflammation and the coagulation fibrinolytic system. The purpose of our research was to evaluate the effect of proprotein convertase subtilisin/kexin type 9 inhibitors (PCSK9i) on lipid parameters and indicators of inflammation, coagulation and fibrinolysis. We included 100 post myocardial infarction (MI) patients with insufficiently controlled LDL-C values despite the maximum dose of statin, and highly elevated Lp(a). Patients received alirocumab or evolocumab (150 mg sc or 140 mg sc every two weeks, respectively), or placebo for 6 months. In patients receiving PCSK9i, a significant decrease in total cholesterol (TC), LDL-C, triglycerides (TG) and Lp(a), and an increase in high density lipoprotein cholesterol (p < 0.001 for all) was found. Before treatment, the concentrations of TC, LDL-C and TG correlated with the concentrations of thrombin activatable fibrinolysis inhibitor (r = 0.41, p < 0.001; r = 0.353, p < 0.001; r = 0.311, p = 0.003, respectively), and plasminogen activator inhibitor-1 (r = 0.302, p = 0.007; r = 0.218, p = 0.049; r = 0.278; p = 0.013, respectively). The concentrations of TC and LDL-C correlated with overall fibrinolytic potential (r = −0.220, p = 0.034; r = −0.207, p = 0.047, respectively). The concentration of TG was related to the concentration of interleukin 6 (r = 0.290, p = 0.004) and interleukin 8 (r = 0.332, p = 0.001). No correlations between Lp(a) and inflammatory or hemostatic variables were found. No associations were found after treatment. Our results show that inflammatory cytokines and fibrinolytic parameters are related to LDL-C and not Lp(a) in post-MI patients before and with neither of them following PCSK9i treatment.
Keywords: inflammation, hemostasis, PCSK9 inhibitors, LDL cholesterol, lipoprotein (a)
Published in DiRROS: 08.06.2026; Views: 254; Downloads: 235
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