Search Results (319)

Metabolic dysfunction-associated steatotic liver disease (MASLD) is characterised by excessive lipid accumulation in hepatocytes and often accompanied by dyslipidaemia. Gynura procumbens, a medicinal plant native to Southeast Asia, exhibits lipid-lowering and hepatoprotective properties. However, its effects on hepatic lipid accumulation and cholesterol metabolism-related gene regulation remain unclear. This study evaluated the effects of G. procumbens extract (GPCE) and stigmasterol on oleic acid-induced hepatocyte steatosis and cholesterol metabolism-related gene expression. GPCE was assessed for HMG-CoA reductase (HMGCR) inhibition, lipid accumulation, and expression of cholesterol metabolism-related genes (HMGCR, SREBP2, LDLR, and PCSK9). Bioassay-guided fractionation identified stigmasterol as a constituent of the highly active fractions and its structure was characterised by LC-TOF-MS and NMR. GPCE and stigmasterol inhibited HMGCR activity by 86.31 ± 5.3% and 56.59 ± 7.6%, respectively. Both treatments reduced lipid accumulation in hepatocytes and modulated the mRNA expression of selected cholesterol homeostasis-related genes, including transcriptional downregulation of SREBP2 and PCSK9. These findings suggest that G. procumbens possesses lipid-lowering activity and that stigmasterol may represent one of the bioactive constituents contributing to its observed biological effects. Further studies involving protein level validation, functional assays and in vivo studies are warranted to fully elucidate the mechanisms and establish the biological relevance of these findings in MASLD. Full article

Background and Objectives: Chronotype and sleep quality are related but non-identical dimensions of sleep health. We examined whether later chronotype is associated with subclinical visceral adiposity and atherogenic dyslipidaemia independently of perceived sleep quality, and whether this association differs by sex, in adults without previously diagnosed chronic disease. Materials and Methods: This single-centre cross-sectional study included 282 adults without previously diagnosed chronic disease or regular medication use. Chronotype was assessed with the Morningness–Eveningness Questionnaire (MEQ) and sleep quality with the Pittsburgh Sleep Quality Index (PSQI). Composite cardiometabolic indices were calculated from routine anthropometric and biochemical data. Primary dependent variables were log-transformed Visceral Adiposity Index (log[VAI]) and Atherogenic Index of Plasma (AIP). Multivariable linear models used heteroscedasticity-consistent type 3 (HC3) robust standard errors and adjusted for age, sex, education, physical activity, and PSQI; body mass index (BMI) was additionally included in the AIP model. Sex × MEQ interactions, false-discovery-rate (FDR) correction, and glycaemic sensitivity analyses were performed. Results: Median age was 28.0 years; 50.4% were women, 25.9% were evening type, and 51.8% had poor sleep quality. Higher MEQ score (greater morningness) was independently associated with lower log(VAI) (B = −0.0096; 95% confidence interval (CI), −0.0159 to −0.0033; β = −0.190; p = 0.003) and AIP (B = −0.0035; 95% CI, −0.0063 to −0.0008; β = −0.160; p = 0.011), whereas PSQI was not independently associated with either outcome. Sex × MEQ interactions were nominally significant and estimates were stronger in women, but interaction terms did not survive FDR correction. Associations persisted after excluding diabetes-range glycaemia but attenuated in strictly normoglycaemic participants. Conclusions: Later chronotype was associated with a less favourable subclinical adiposity–atherogenic profile independently of perceived sleep quality. Findings are cross-sectional, and the sex-specific pattern is hypothesis-generating. Prospective studies with objective circadian, sleep, dietary-timing, behavioural, and hormonal measures are required. Full article

Objectives: Despite successful antiretroviral treatment (ART), people living with HIV (PWH) continue experiencing chronic immune activation and comorbidities. We analysed whether the Fibrosis 4 index (FIB-4) is associated with monocyte–macrophage activation in PWH with non-severe hepatic disease. Materials and Methods: We performed a cross-sectional analysis about factors associated with monocyte–macrophage activation among PWH either on triple or dual ART. Background measurements, comorbid conditions and FIB-4 values were correlated with plasmatic markers of monocyte–macrophage activation (sCD163 and sCD14) using univariate and linear regression analysis. Results: We included 366 subjects (age 60.5, 75% male, years of HIV infection 24.5, mean FIB-4 1.52, 8% with FIB-4 > 2.67, Body Mass Index 24.5). In univariate analysis, FIB-4 was associated with older age, years of HIV infection, ART duration, lower CD4/CD8 ratio at inclusion, lower nadir CD4, higher sCD14 and sCD163 values, living alone, dyslipidaemia, high blood pressure and diabetes (p < 0.05 for all). In multivariate analysis FIB-4 ≥ 1.3 was associated with sCD163 values ≥ 782 ng/mL [AdjOR 1.85, 95% CI [1.05; 3.33] p = 0.035], independently from CD4 count, ART duration, living alone, hepatitis C, high blood pressure and alcohol. Conclusions: The FIB-4 is a simple tool reliable for monocyte–macrophage activation in PWH, able to define subjects with higher risks of complications. Full article

Cardiovascular disease (CVD) remains the leading cause of morbidity and mortality worldwide, and lowering low-density lipoprotein cholesterol (LDL-C) remains a cornerstone of cardiovascular prevention. Statins are among the most extensively studied and widely prescribed medications and have demonstrated substantial benefits in reducing major adverse cardiovascular events in both primary and secondary prevention settings. Nevertheless, the effectiveness of statin therapy in routine clinical practice is frequently compromised by poor adherence, treatment discontinuation, concerns regarding adverse effects, and persistent residual cardiovascular risk. This narrative review synthesises contemporary evidence relating to the mechanisms of action of statins, their role in primary and secondary prevention, determinants of medication adherence, statin-associated muscle symptoms (SAMSs), and emerging developments in precision cardiovascular medicine. Current evidence indicates that although statins remain highly effective in reducing cardiovascular risk, long-term treatment success is strongly influenced by behavioural, psychological, social, and healthcare system factors. Increasing attention has also been directed towards the multifactorial nature of SAMSs and the contribution of nocebo effects to perceived statin intolerance. Emerging approaches involving pharmacogenomics, artificial intelligence, digital health technologies, and multidimensional risk assessment offer opportunities for more individualised prevention strategies, although important limitations relating to cost, accessibility, and external validity remain. Overall, contemporary cardiovascular prevention requires a patient-centred approach that integrates biological, behavioural, and social determinants of health to optimise treatment adherence and improve long-term cardiovascular outcomes. Full article

Background/Objectives: European guidelines recommend increasingly stringent, risk-stratified low-density lipoprotein cholesterol (LDL-C) targets, but real-world attainment remains suboptimal. We evaluated 12-month lipid-target attainment and changes in model-derived cardiovascular risk estimates in an ambulatory dyslipidaemia cohort. Methods: In this prospective, single-centre observational study, 101 consecutive adults were assessed at baseline and after at least 12 months of routine-care lipid-lowering therapy. Patients were classified as moderate/low, high, or very high cardiovascular risk. The primary endpoint was attainment of the risk-specific LDL-C target at 12 months versus baseline. Paired changes were tested using the McNemar exact and Wilcoxon signed-rank tests. Multivariable logistic regression assessed correlates of target attainment, with Firth penalisation used because of sparse outcomes in the higher risk strata. Results: LDL-C target attainment increased from 6.0% to 43.0%, and non-HDL-C attainment from 7.0% to 51.5% (both p < 0.001). At 12 months, 89% of moderate/low-risk patients reached the LDL-C target, compared with 9% of high-risk and 23% of very-high-risk patients (p < 0.001). Higher risk category was strongly associated with non-attainment, although the odds ratios were imprecise because of sparse events. Only one patient received a high-intensity statin and three received a PCSK9 inhibitor, despite 63% of the cohort being at high or very high risk. Model-derived risk scores decreased, partly as a mathematical consequence of updated lipid inputs. Therapy was well tolerated. Conclusions: Lipid control improved substantially, but target attainment remained poorest in patients at greatest cardiovascular risk. Earlier treatment intensification, structured adherence assessment, and more consistent use of combination therapy may reduce this implementation gap. Full article

Background: Coronary artery disease (CAD) arises from the convergence of genetic susceptibility, lipid dysregulation, and modifiable environmental exposures. The polymorphism rs4977574, located proximal to the CDKN2A/CDKN2B gene cluster, has been repeatedly implicated in CAD risk across several populations, yet its relationship to intermediate cardiometabolic phenotypes and pharmacological treatment patterns in Saudi individuals remains poorly characterized. Objective: This study aimed to evaluate the association of rs4977574 with CAD status, lipid-related phenotypes, smoking history, obesity, and atorvastatin exposure in a Saudi cardiovascular cohort, and to assess the robustness of observed associations through sensitivity-adjusted analyses excluding participants with major metabolic confounders. Methods: A case–control genetic association study was conducted in Saudi participants with clinically confirmed CAD and healthy controls. Genomic DNA was genotyped for rs4977574 using TaqMan^® allelic discrimination assays. Genotype–phenotype associations were examined using chi-square testing, binary logistic regression under additive and dominant inheritance models, and one-way ANOVA for continuous lipid traits. Hardy–Weinberg equilibrium (HWE) was assessed in controls. Sensitivity analyses were conducted by sequentially excluding participants with obesity, smoking, diabetes mellitus, hypertension, dyslipidaemia, and statin use. Results: After covariate adjustment, rs4977574 was not independently associated with CAD case–control status under any inheritance model. Genotype-stratified analyses identified significant differences in HDL-cholesterol and triglyceride concentrations among cases, with no equivalent effects on total cholesterol or LDL-cholesterol. A significant association was observed between rs4977574 genotype and atorvastatin prescribing patterns. Sensitivity-adjusted analyses were directionally consistent with primary findings. HWE deviation persisted in controls after sequential metabolic exclusions, implicating population stratification or regional genetic heterogeneity rather than sample selection bias. Conclusions: Although rs4977574 did not associate independently with CAD susceptibility, its relationship with HDL-cholesterol, triglycerides, and atorvastatin exposure indicates that this locus contributes to cardiometabolic phenotypic heterogeneity in this Saudi cohort. These findings support phenotype-oriented and pharmacogenetically informed approaches in regional cardiovascular genetics and highlight the need for larger, ancestry-stratified investigations across Middle Eastern populations. Full article

Background/Objectives: The management of dyslipidaemia in Slovakia has undergone significant changes in recent years, particularly through the relaxation of prescription restrictions for existing medications and the introduction of new innovative molecules. Achieving target levels of LDL cholesterol (LDL-C) plays a key role in preventing the onset and progression of atherosclerosis-related cardiovascular (CV) diseases. The aim of this study was to analyse how these changes have affected the effectiveness of reaching target LDL-C levels in patients at very high CV risk. Methods: This project was conducted as a retrospective analysis of anonymised LDL-C values from 2020 to 2023 using data from a collaborating nationwide laboratory. Patients included were those diagnosed with acute coronary syndrome (ACS), stroke, and, more generally, those with high and very high CV risk. Target LDL-C values were assessed based on the 2019 ESC/EAS guidelines. Results: A total of 363,020 LDL-C test records from 115,950 patients were evaluated over the four-year study period. Among patients diagnosed with ACS, 2.2–5% achieved target LDL-C levels in the respective years of observation 2020–2023. As many as 6.5–7.4% had LDL-C levels ≥ 4.9 mmol/L. For patients with stroke, only 4–6.6% reached target LDL-C levels, while 5.6–6.7% had levels ≥ 4.9 mmol/L. In the group with very high CV risk, only 1.7–3% achieved target levels, and 7.5–8.7% had extremely high LDL-C levels ≥ 4.9 mmol/L. Despite these modest improvements, over 93.4% of patients in the highest-performing subgroup failed to reach the absolute guideline target threshold in 2023. Conclusions: While the lifting of prescription constraints and the introduction of innovative treatments correlates with a doubling of absolute target attainment and a contraction of extreme hypercholesterolemia, overall control remains critically low in Slovakia. Systematic, protocol-driven combination regimens and intensive follow-up are urgently needed. Full article

Cardiovascular disease (CVD) remains the leading cause of mortality worldwide, and residual inflammatory risk persists despite optimal lipid and glucose control. Emerging evidence indicates that metabolic reprogramming within immune cells constitutes a central driver of cardiovascular immune injury. In this review, we propose a unifying framework in which glyco-lipotoxicity acts as a primary metabolic trigger, inducing mitochondrial dysfunction, oxidative stress, and activation of the NLRP3 inflammasome and cGAS–STING pathways. Hyperglycaemia and dyslipidaemia reshape intracellular metabolic circuits, enhancing glycolysis and disrupting oxidative phosphorylation, thereby promoting sustained pro-inflammatory phenotypes. Crucially, metabolic intermediates function as cofactors for epigenetic remodelling. This establishes trained immunity in both circulating innate immune cells and haematopoietic stem/progenitor cells, which serves as the cellular basis for persistent metabolic memory. This persistent immunometabolic imprint amplifies sterile inflammation and accelerates vascular and myocardial remodelling. Furthermore, these processes are systemically propagated through cross-organ communication networks, including the heart–adipose, gut–heart, and cardio-hematopoietic axes, forming a multidimensional inflammatory amplification loop. We also summarise emerging therapeutic strategies targeting the metabolic–epigenetic axis, aiming to reverse maladaptive trained immunity and mitigate residual CVD risk. By integrating immunometabolism, epigenetic regulation, and organ crosstalk, this review highlights metabolic reprogramming as a pivotal mechanistic nexus and potential precision target for cardiovascular protection. Full article

Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in reproductive-aged women. Epidemiologic evidence increasingly indicates that women with PCOS exhibit elevated risk of ischaemic stroke. Unlike prior reviews that have focused predominantly on general cardiovascular risk in PCOS, this review specifically examines ischaemic stroke risk, its mechanistic links, and the extent to which current stroke and cardiovascular frameworks fail to account for PCOS. We conducted a narrative review examining the association of PCOS on ischaemic stroke and cardiovascular disease (CVD). Large-scale cohort studies and meta-analyses from 2000 to 2025 were identified from Medline, Embase, PubMed, and Google Scholar, with specific emphasis on ischaemic stroke in women with PCOS. Case reports and case series were excluded. There is substantial evidence supporting the relationship between PCOS and increased vascular risk. Large-scale cohort studies and meta-analyses report higher rates of cerebrovascular events among women with PCOS. A recent 2025 meta-analysis pooling 11 studies reported a statistically significantly increased risk of stroke in women with PCOS (OR = 1.89, 95% CI = 1.22–2.55), although heterogeneity was high (I² = 97.7%), indicating important variation in study design, populations, and confounder adjustment. Other meta-analyses report more modest associations, and some studies did not demonstrate significant associations with myocardial infarction or all-cause mortality. Several analyses also showed attenuation of risk following adjustment for body mass index and metabolic factors. The observed association between PCOS and vascular risk should be interpreted with caution, given substantial heterogeneity and potential confounding by cardiometabolic factors. These findings raise the possibility that increased risk may be mediated through established pathways such as obesity, insulin resistance, and dyslipidaemia rather than representing a consistently independent effect. Despite this, PCOS remains inconsistently recognised within clinical frameworks. Current stroke guidelines and widely used risk prediction tools, including QRISK3 and the Essen Stroke Risk Score, do not incorporate PCOS, highlighting a potential gap in sex-specific risk assessment. Evidence demonstrating that inclusion of PCOS improves risk prediction or clinical outcomes remains limited. However, under-recognition of vascular risk in women with PCOS may limit timely risk assessment and intervention. This review highlights a number of implementation gaps globally, including gaps in research and inter-disciplinary communication. Priority next steps include prospective studies to clarify whether PCOS independently contributes to vascular risk, and predictive modelling studies to determine whether including PCOS improves risk stratification. In parallel, multidisciplinary care pathways may support earlier identification and prevention in higher-risk women. Full article

This case highlights a novel genotype–phenotype correlation in the field of endocrinology. Specific endocrine and imaging assessment, in addition to next-generation sequencing (NGS), was performed on the Illumina MiSeq platform, using a TruSight One Sequencing Panel kit for genomic analysis of coding regions of 4813 genes. A 54-year-old female was confirmed with a papillary thyroid carcinoma after total thyroidectomy and underwent radioiodine ablative therapy. Three years later, a left femoral enchondroma of almost 3 cm was identified at computed tomography (CT) scan and magnetic resonance imaging (MRI). She experienced hypertension (in addition to obesity, dyslipidaemia and impaired glucose tolerance) and was later confirmed with ACTH-independent cortisol excess [lack of cortisol suppression at 1 mg dexamethasone testing of 13.9 (normal < 1.8 µg/dL)], noting bilateral adrenal tumors, of 4.7 cm (right), respectively, and of 1.6 cm (left) at CT. Right laparoscopic adrenalectomy was performed with post-operative adrenal insufficiency, requiring glucocorticoid replacement and stopping the anti-hypertensive medication. Pathology report confirmed an adrenocortical adenoma (a Ki67 proliferation index of 2%). Noting the unusual association of the mentioned conditions, NGS was performed in the peripheral blood and identified a heterozygote missense variant of the APC gene (c.5759G>A, p.Arg1920Gln), a heterozygote missense variant of the MSH6 gene (c.2092C>G, p.Gln698Glu), and an incidental additional finding: a heterozygote stop gain pathogenic variant of the CACNA1S gene (c.2707C>T, p.Arg903*). The first two are currently classified as variants of uncertain significance. Whether the co-presence of a triple mutation may change the clinical picture and the life-long outcomes across reciprocal influence is still an open matter. Further research will point out the clinical implications of this genotype–phenotype association, which, to our best knowledge, has not been previously reported. Full article

Background: Μetabolic syndrome (MetS)—comprises central adiposity, elevated blood pressure, dyslipidaemia, and dysglycaemia, increasing the risk of type 2 diabetes and cardiovascular disease. Exercise training improves cardiorespiratory fitness and several MetS components, but real-world effectiveness is limited by poor adherence, restricted supervision, and insufficient personalisation. Objective: This scoping review mapped the clinical intervention evidence on technology-enhanced exercise and structured physical activity relevant to MetS, while distinguishing direct MetS evidence from translational evidence. Methods: In accordance with PRISMA-ScR, we searched PubMed and extended the search to Scopus and Web of Science; a supplementary IEEE Xplore search and a post hoc Embase check were also conducted. Eligible studies were interventions using web-based delivery, wearables, telemonitoring/mobile health (mHealth), artificial intelligence (AI) coaching, virtual reality (VR)/exergaming, or continuous glucose monitoring (CGM) alongside exercise training or structured physical activity. Results: Nineteen studies met the eligibility criteria. The evidence base was weighted toward wearable/app-based feedback and telemonitoring/mHealth/web-based approaches, with fewer studies on VR/exergaming, CGM-enabled exercise, and AI coaching. Most studies were randomised or cluster-randomised, but interventions were usually short term. Across categories, technology most consistently supported adherence, self-monitoring, accountability, remote supervision, and, in selected cases, physiology-informed personalisation. Direct MetS evidence was strongest for wearables with structured feedback, telemonitoring, mHealth, and web-based delivery, whereas AI coaching and CGM were supported by adjacent translational evidence. Conclusions: Technology-enhanced exercise and structured physical activity show promising but heterogeneous and still preliminary potential for MetS management. Key limitations include short follow-up, uneven representation across categories, inconsistent reporting of exercise dose/intensity fidelity and adverse events, and limited equity and implementation outcomes. Full article

Hypoxia activates hypoxia-inducible factors (HIFs), which regulate genes involved in erythropoiesis, angiogenesis, and metabolism. HIF stability is controlled by oxygen-dependent HIF prolyl 4-hydroxylases (HIF-P4Hs). Pharmacological HIF-P4H inhibitors are approved for the treatment of anaemia in chronic kidney disease (CKD). Beyond erythropoiesis, these drugs have been linked to improved lipid profiles in CKD, and preclinical studies suggest benefits for glucose tolerance and cardiovascular protection. However, cardiometabolic effects of HIF-P4H inhibitors have not been systematically examined in healthy or non-anaemic individuals. This investigator-initiated, double-blind, placebo-controlled, randomised crossover trial evaluates the systemic effects of roxadustat, an orally administered pan-HIF-P4H inhibitor. The study consists of two 10-day study arms separated by a minimum 4-week washout. Participants receive 70 mg of roxadustat or a placebo thrice a week. The primary hypothesis is that roxadustat lowers plasma total cholesterol. Secondary outcomes include changes in LDL cholesterol, triglycerides, insulin sensitivity, glucose tolerance, body composition, 24 h blood pressure, exercise capacity, autonomic cardiovascular regulation, and skeletal muscle microcirculation. Healthy volunteers (n = 24) aged 18–40 years will be enrolled. This study will provide insights into the potential of HIF-P4H inhibitors for obesity, dyslipidaemia, insulin resistance, and hypertension, and may inform future therapeutic strategies for metabolic syndrome, type 2 diabetes, and cardiovascular disease. Full article

Background/Objectives: Background: Dyslipidaemia and oxidative stress (OS) are frequent in peritoneal dialysis (PD). The Lipoprotein Combine Index (LCI) integrates lipid parameters, but its relationship with peritoneal transport and OS is unclear. Methods: This cross-sectional study included 100 clinically stable adults on continuous ambulatory PD with preserved ultrafiltration and adequate dialysis. LCI was calculated as (total cholesterol × triglycerides × LDL-C)/HDL-C and analyzed by tertiles. Lipid peroxidation and antioxidant markers were measured in serum, erythrocytes, urine, and spent dialysate. Multivariable regression models examined associations between LCI, peritoneal solute transport, and dialysate OS markers. Results: Higher LCI was independently associated with lower peritoneal solute transport. LCI correlated inversely with the 4 h dialysate-to-plasma creatinine ratio (ρ = −0.32, p = 0.001) and remained significant after adjustment (adjusted R² = 0.224, p < 0.001). Increasing LCI was associated with higher malondialdehyde levels in serum, urine, and dialysate (all p ≤ 0.008) and impaired antioxidant defenses, including lower total peroxidase activity in erythrocytes and dialysate (both p = 0.001), reduced serum sulfhydryl groups (p = 0.011), decreased oxidative resistance of erythrocytes, and increased peroxide-induced hemolysis (both p = 0.001). In adjusted models, logLCI was independently associated with higher dialysate malondialdehyde (p < 0.001) and lower dialysate peroxidase activity (p = 0.005). Conclusions: In clinically stable PD patients, higher lipid burden assessed by LCI is independently associated with lower peritoneal solute transport and a marked increase in systemic and local OS. Our findings suggest that dyslipidaemia may contribute to early metabolic and oxidative changes even before overt peritoneal membrane dysfunction develops. Full article

Dendrobium officinale (DO) is a traditional medicinal and edible plant whose polysaccharides help modulate gastrointestinal and metabolic functions. Fresh DO is commonly processed into “Fengdou” to prolong shelf life, but the effects of this processing on polysaccharide structure and bioactivity remain unclear. In this study, polysaccharides from fresh DO (FDOP) and Fengdou (DDOP) were isolated, purified, and comparatively characterized. Based on structural analyses, FDOP and DDOP have similar functional groups and O-acetylated pyranosyl structures in both polysaccharides, which are identified as mannose–glucose heteropolysaccharides. However, FDOP was characterized by a higher mannose-to-glucose ratio (79.77:19.57) and molecular weight (187.1 kDa), as well as a more structurally diversified →4-linked backbone. In contrast, DDOP contained more glucose (68.74:30.94) and exhibited a lower molecular weight (125.1 kDa) and simplified backbone. In zebrafish models, both polysaccharides were found to alleviate loperamide-induced constipation and reduce lipid accumulation. DDOP showed stronger constipation-relieving activity, whereas FDOP exerted more pronounced hypolipidaemic effects, which can be ascribed to the higher molecular weight, mannose enrichment, and more complex backbone structure. These findings provide a structural basis and theoretical support for developing DO-derived polysaccharides as functional food ingredients targeting constipation and dyslipidaemia. Full article

Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most common liver disease worldwide, with an estimated global prevalence of 38% in adults. MASLD confers a significant increase in morbidity and mortality due to its association with cardiovascular disease and progressive liver disease, including cirrhosis and hepatocellular carcinoma. Current treatment paradigms for MASLD are centred around lifestyle modification and weight loss, with a need for pharmacotherapeutic options. Given the strong relationship between MASLD and cardiovascular disease, there is an interest in evaluating the efficacy and safety of cardiovascular medications such as statins in liver disease. Statins are the most commonly prescribed lipid-lowering medication in the world, with an established role in reducing cardiovascular morbidity and mortality. Statins are currently under-prescribed in the MASLD patient population, yet there is growing interest in determining whether statins could be utilised to treat MASLD itself. This comprehensive review aims to explore the evidence regarding the use of statin therapy for conventional, lipid-lowering indications in patients with MASLD and its potential benefits for the treatment of MASLD and its complications. Full article