Osteoarthritis (OA) is one of the most common and burdensome musculoskeletal disorders and a major cause of pain, disability, and reduced quality of life worldwide. In recent years, increasing attention has been paid to extra-articular factors influencing its development and progression, opening new avenues of research into pathophysiological mechanisms and potential therapies. One of the most promising areas concerns the role of the gut–joint axis and related alterations in the gut microbiome. Numerous studies indicate that an imbalance of gut bacteria, increased intestinal permeability, and low-grade inflammation may contribute to the progression of degenerative joint processes. The mechanisms through which the microbiota influences the immune system and host metabolism are becoming increasingly well understood, including pathways involving short-chain fatty acids, tryptophan metabolites, and bile acids. Despite growing evidence linking dysbiosis to the pathogenesis of OA, effective therapeutic strategies based on microbiome modulation remain under active investigation. Among the most frequently studied approaches are probiotics, dietary interventions, and more advanced strategies such as gut microbiota transplantation and targeted modulation of microbial metabolites. However, before these methods can become part of routine treatment, extensive clinical trials and a clearer understanding of causal relationships between the microbiome and joint degeneration are required. This article summarises the current state of knowledge regarding the role of the gut microbiome in osteoarthritis, outlines key research findings, and highlights current and potential therapeutic directions.

There is a widely known relationship between certain microbes and cancer progression. For instance, Helicobacter pylori is associated with the occurrence of gastric cancer, while HPV is associated with cervical and head and neck cancers. Recent studies have uncovered novel and important associations between bacterial presence and tumor formation and treatment response. Apart from the influence of the intestinal microbiome on cancer, the local activity of bacteria affects disease properties as well. Bacteria can localize within tumors in less vascularized niches. Their presence mediates the activity of signaling pathways, which contribute to tumorigenesis. Furthermore, they affect the composition of the tumor microenvironment, a highly complex structure composed of immunoregulatory cells and secreted inflammatory mediators. Recently, researchers have analyzed the properties of bacteria to develop novel anticancer strategies. The aim of this review is to discuss the latest findings regarding the relationships between bacteria and cancer and the properties of bacteria that could be used to kill cancer cells.

Rheumatoid arthritis (RA) is a progressive autoimmune disease leading to structural and functional joint damage and, eventually, to physical disability. The pathogenesis of the disease is highly complex and involves interactions between fibroblast-like synoviocytes (FLSs) and immune cells, which stimulate the secretion of pro-inflammatory factors, leading to chronic inflammation. In recent years, studies have demonstrated the importance of epigenetics in RA. Specifically, epigenetic alterations have been suggested to serve as diagnostic and treatment biomarkers, while epigenetic mechanisms are thought to be involved in the pathogenesis of RA. Epigenetic regulators coordinate gene expression, and in the case of inflammatory diseases, they regulate the expression of a broad range of inflammatory molecules. In this review, we discuss current evidence on the involvement of DNA and RNA methylation in RA.

The macrophage immunometabolism regulator (MACIR) gene, also known as C5orf30, has emerged as a potential regulator of immune responses and inflammatory processes. Increasing evidence suggests that MACIR gene expression is associated with macrophage function, cellular metabolism, and inflammatory signalling, potentially contributing to the maintenance of immune homeostasis. Dysregulation of MACIR gene expression has been associated with pathological inflammatory responses and may play a role in the development and progression of autoimmune and chronic inflammatory diseases, particularly rheumatoid arthritis. However, the molecular mechanisms underlying the biological functions of MACIR remain incompletely understood. This review summarises current knowledge regarding the structure, expression, and regulation of the MACIR gene, with particular emphasis on its potential role in immune cell function and inflammatory signalling. The involvement of MACIR in rheumatoid arthritis and other immune-mediated diseases is discussed, together with emerging evidence linking MACIR to immunometabolism and disease-associated cellular responses. Furthermore, the potential of MACIR as a biomarker and therapeutic target is considered. A better understanding of the mechanisms regulating MACIR gene expression may provide new insights into the pathogenesis of inflammatory and autoimmune diseases and contribute to the development of novel diagnostic and therapeutic strategies.

Hypertensive nephropathy (HN) is a leading cause of chronic kidney disease and end-stage renal disease worldwide and results from the long-term effects of hypertension on renal structure and function. The pathogenesis of HN is complex and involves haemodynamic disturbances, renal vascular injury, oxidative stress, chronic inflammation, and progressive interstitial fibrosis. In recent years, increasing attention has focused on the role of non-coding RNAs (ncRNAs)—including microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs)—as key regulators of gene expression involved in these processes. This review summarises the current understanding of the molecular mechanisms underlying HN, with particular emphasis on the roles of oxidative stress, activation of the renin–angiotensin–aldosterone system, transforming growth factor beta signalling, and inflammatory and fibrogenic pathways. The contribution of dysregulated ncRNAs to endothelial dysfunction, inflammatory responses, apoptosis, angiogenesis, and renal remodelling and fibrosis is also discussed. Particular attention is given to miRNAs and lncRNAs as mediators of disease progression and potential biomarkers, as well as to the emerging role of circRNAs in hypertensive kidney injury, including their involvement in the regulation of redox balance and intercellular communication. Collectively, available evidence indicates that ncRNAs represent a critical link between haemodynamic stimuli and persistent molecular alterations in renal tissue, highlighting their potential as diagnostic markers and therapeutic targets in HN.