Current Pharmaceutical Design - Volume 32, Issue 9, 2026

This review explores the critical role of mitochondria in the immunometabolic processes underlying rheumatoid arthritis (RA) and osteoarthritis (OA). It examines the interplay between immune cells, metabolic demands, and tissue environments, emphasizing the impact of bioenergetics on immune responses and disease progression. Mitochondrial dysfunction in chondrocytes and immune cells contributes to OA and RA through mechanisms such as oxidative stress, disrupted calcium homeostasis, and inflammasome activation. In OA, mitochondrial dysfunction in chondrocytes results in impaired energy production, elevated reactive oxygen species (ROS), and calcium imbalance, leading to cartilage degradation and inflammation. The review highlights how disturbances in the mitochondrial respiratory chain and apoptotic pathways drive joint tissue damage. In contrast, RA shows how mitochondrial dysfunction influences chronic inflammation and synovial hyperplasia. The role of mitochondrial DNA (mtDNA) as a damage-associated molecular pattern (DAMP) is emphasized, illustrating how oxidized mtDNA activates inflammatory pathways, triggers immune responses, and contributes to joint destruction. Additionally, mitochondrial genetic variations may exacerbate inflammation and oxidative stress in RA. The review also discusses the effects of various RA treatments-conventional synthetic anti-rheumatic drugs, biological agents, and targeted synthetic DMARDs-on mitochondrial function. Insights into how these therapies modulate mitochondrial pathways and oxidative stress in immune and joint cells highlight new potential treatment strategies. This review enhances our understanding of OA and RA pathophysiology by elucidating the connections between mitochondria, immune responses, and rheumatic diseases, paving the way for innovative therapies targeting mitochondrial dysfunction.

MicroRNAs (miRNAs) are the regulators of gene expression and several cellular processes related to the immune system. miRNAs during tuberculosis (TB) infection are considered regulatory factors for the host immune system. Mycobacterium tuberculosis has a great ability to survive and multiply in phagocytic cells, which makes it difficult to treat. It can replicate through various cellular pathways. To establish the infection in the host cell, M. tuberculosis changes in the miRNA expression and increases survival capacity with high infectivity. miRNAs are widely used as biomarkers and therapeutic agents for tuberculosis. During M. tuberculosis infection, altered miRNA expressions can cause the progression of the disease and discriminate between latent and active TB infection. Due to their active involvement in disease progression, miRNAs may be utilized as potential biomarkers. Furthermore, the involvement of miRNA in autophagy and apoptosis modulation against M. tuberculosis highlights its potential for host-directed therapy. In this review article, we attempt to summarize the expression and role of various miRNAs in TB as immune modulators, differential activators between different phases of TB, including neuronal dysfunction in the brain, as therapeutic targets and diagnostic tools against TB.

Despite significant advancements in medical science, cancer continues to be a major cause of morbidity and mortality worldwide. A key factor contributing to this persistent burden is the emergence of resistance to conventional therapeutic modalities, including chemotherapy, radiation therapy, and surgery. This phenomenon of drug resistance significantly hampers the efficacy of these treatments, leading to therapeutic failure and poor clinical outcomes. A detailed understanding of the molecular and cellular mechanisms underlying drug resistance is crucial for devising targeted strategies to overcome these barriers. In this review, we aim to critically assess and highlight various approaches that can effectively reduce chemotherapy resistance, with the goal of improving the therapeutic efficacy of chemotherapy and enhancing overall patient survival.

Oral diseases represent significant health challenges, with periodontal diseases and dental caries ranking as key preventable infectious diseases worldwide. Oral health affects overall quality of life, and inadequate oral hygiene is associated with chronic diseases. Carvacrol is a monoterpenoid phenol found in essential oils of pepperwort (Lepidium flavum), thyme (Thymus vulgaris), oregano (Origanum vulgare), wild bergamot (Citrus aurantium), and other plants. Carvacrol exhibits numerous biological activities, including antimicrobial, antioxidant, and anticancer effects. Carvacrol demonstrated the ability to inhibit the oral pathogens examined and exhibited properties that prevent biofilm formation on their oral biofilm; thus, it may be used to manage and prevent the colonization of microorganisms, which is particularly important in human oral diseases. Besides, carvacrol protects gingival tissue in periodontal disease. Knowledge of carvacrol's many actions will help develop novel treatment plans, and designing clinical studies will optimize its potential advantages for treating oral diseases.