Cardiovascular diseases (CVDs) are a leading cause of global morbidity and mortality, significantly driven by chronic inflammation. Interleukin-6 (IL-6) and interleukin-1β (IL-1β) are critical inflammatory cytokines implicated in CVD progression. This systematic review evaluates the roles of IL-6 and IL-1β in CVDs by synthesizing data from relevant studies to understand their impact on cardiovascular outcomes and identify potential therapeutic interventions. A comprehensive literature search was conducted using PubMed and Embase, covering studies from January 2014 to December 2024. Inclusion criteria encompassed studies investigating IL-6 and/or IL-1β in CVDs, including human and relevant animal models, and reporting clinical outcomes, molecular mechanisms, or therapeutic interventions. Data extraction and quality assessment were performed independently by two reviewers. Our review included 12 studies focusing on the roles of IL-6 and IL-1β in various CVDs. Elevated IL-6 levels were significantly associated with peripheral artery disease, myocardial infarction, and heart failure, while IL-1β levels were linked to worse outcomes in coronary artery disease and heart failure. Meta-analyses indicated a significant association between higher IL-6 and IL-1β levels and increased risk of adverse cardiovascular events. These findings suggest that targeting IL-6 and IL-1β could offer promising therapeutic strategies for reducing inflammation and improving cardiovascular outcomes.

Hashimoto’s thyroiditis (HT) and alopecia areata (AA) are organ-specific autoimmune diseases that frequently co-occur, suggesting shared immunological and microbial pathways. The gut microbiome has emerged as a key modulator of immune function, yet disease-specific microbial signatures remain poorly defined. Fecal samples from 51 participants (HT: n = 16, AA: n = 17, healthy controls: n = 18) aged 18–65 years were analyzed using shotgun metagenomic sequencing followed by multivariate statistical analyses. While alpha and beta diversity did not differ significantly across groups, taxonomic profiling revealed disease-specific microbial patterns. Bacteroides fragilis was significantly enriched in HT, suggesting a potential role in immune modulation; although mechanisms such as polysaccharide A production and molecular mimicry have been proposed in previous studies, their involvement in HT remains to be confirmed. Microbacterium sp. T32 was elevated in both HT and AA, indicating its potential as a shared autoimmune marker. Functional analysis showed increased fermentation and amino acid biosynthesis in AA, contrasting with reduced metabolic activity and elevated carbohydrate biosynthesis in HT. HT and AA exhibit distinct gut microbial and metabolic signatures. Bacteroides fragilis and Microbacterium sp. T32 may serve as potential microbial correlates for autoimmune activity, offering new insights into disease pathogenesis and targets for microbiome-based interventions.

The gut microbiome is known to modulate metabolic health, yet its role in coronary heart disease (CHD) and heart failure with preserved ejection fraction (HFpEF) remains unclear. In the present study, we profiled the gut microbiome of 234 participants using shotgun metagenomic sequencing across controls ( n = 43), individuals with low-risk atherosclerosis (LRAS, n = 23), and patients with CHD + HFpEF ( n = 168). Species richness was significantly increased in CHD + HFpEF, with no disruption in taxonomic evenness. LRAS did not diverge significantly in alpha metrics. In contrast, beta diversity analysis demonstrated significant divergence of both LRAS and CHD + HFpEF taxonomic structure from controls, with the greatest divergence in CHD + HFpEF, particularly in older patients. Notably, all differences were attenuated when comparing obese controls and disease groups. However, significant heterogeneity in multivariate dispersion was observed, and a contribution of differences in variation cannot be excluded. Further differential analysis, adjusting for age, BMI, sex, and glucose and lipid profiles, revealed significant associations between specific taxa and CHD + HFpEF, including depletion of the saccharolytic fermenter Bifidobacterium and enrichment of taxa linked to proteolytic or inflammatory metabolism (notably Prevotella and Bilophila ), regardless of age and BMI. Subsequent analysis of inferred functional features indicated increased potential for L-citrulline, L-glutamate, L-lysine, and pyrimidine metabolism in CHD + HFpEF. Collectively, the present analysis suggests that CHD + HFpEF is associated with distinct compositional and functional shifts in the gut microbiome. Further longitudinal and interventional research is required to determine which of these microbial features contribute to disease progression and to better characterize underlying mechanisms.