Pathophysiology, Diagnosis, and Management of Takayasu Arteritis: A Review of Current Advances.

Takayasu arteritis (TA) is a rare, chronic, inflammatory vasculitis that primarily affects large arteries, causing significant morbidity and mortality. This review provides an overview of the pathophysiology, diagnosis, and management of TA based on current advances in the field. TA is characterized by autoimmune-mediated inflammation, vascular remodeling, and endothelial dysfunction. The disease progresses through three stages (active, chronic, and healing phase) each presenting distinct clinical features. Diagnosis of TA can be challenging due to non-specific clinical manifestations and the lack of specific diagnostic tests. Various imaging modalities, such as angiography, ultrasound, and Doppler techniques, play a crucial role in the diagnosis of TA by visualizing arterial involvement and assessing disease extent. Management of TA involves a multidisciplinary approach, with disease-modifying anti-rheumatic drugs (DMARDs) as the cornerstone of medical therapy. Synthetic and biologic DMARDs are used to induce remission, control inflammation, and prevent complications. Non-pharmacologic interventions, such as resistance exercises and curcumin supplementation, show potential benefits. Invasive interventions, including endovascular therapy and open surgery, are used for managing vascular lesions. However, challenges remain in disease understanding and management, including the heterogeneity of disease presentation and the lack of standardized treatment guidelines. The future of TA management lies in precision medicine, utilizing biomarkers and molecular profiling to personalize treatment approaches and improve patient outcomes. Further research is needed to unravel the underlying mechanisms of TA and develop targeted therapies.

Biomimetic Approaches in Cardiac Tissue Engineering: Replicating the Native Heart Microenvironment.

Cardiovascular diseases, including heart failure, pose significant challenges in medical practice, necessitating innovative approaches for cardiac repair and regeneration. Cardiac tissue engineering has emerged as a promising solution, aiming to develop functional and physiologically relevant cardiac tissue constructs. Replicating the native heart microenvironment, with its complex and dynamic milieu necessary for cardiac tissue growth and function, is crucial in tissue engineering. Biomimetic strategies that closely mimic the natural heart microenvironment have gained significant interest due to their potential to enhance synthetic cardiac tissue functionality and therapeutic applicability. Biomimetic approaches focus on mimicking biochemical cues, mechanical stimuli, coordinated electrical signaling, and cell-cell/cell-matrix interactions of cardiac tissue. By combining bioactive ligands, controlled delivery systems, appropriate biomaterial characteristics, electrical signals, and strategies to enhance cell interactions, biomimetic approaches provide a more physiologically relevant environment for tissue growth. The replication of the native cardiac microenvironment enables precise regulation of cellular responses, tissue remodeling, and the development of functional cardiac tissue constructs. Challenges and future directions include refining complex biochemical signaling networks, paracrine signaling, synchronized electrical networks, and cell-cell/cell-matrix interactions. Advancements in biomimetic approaches hold great promise for cardiovascular regenerative medicine, offering potential therapeutic strategies and revolutionizing cardiac disease modeling. These approaches contribute to the development of more effective treatments, personalized medicine, and improved patient outcomes. Ongoing research and innovation in biomimetic approaches have the potential to revolutionize regenerative medicine and cardiac disease modeling by replicating the native heart microenvironment, advancing functional cardiac tissue engineering, and improving patient outcomes.

Novel Therapeutic Targets for Fibrodysplasia Ossificans Progressiva: Emerging Strategies and Future Directions.

Fibrodysplasia ossificans progressiva (FOP), also known as Stoneman syndrome, is a rare genetic disorder characterized by abnormal bone development caused by activating mutations of the ACVR1 gene. FOP affects both the developmental and postnatal stages, resulting in musculoskeletal abnormalities and heterotopic ossification. Current treatment options for FOP are limited, emphasizing the need for innovative therapeutic approaches. Challenges in the development of management criteria for FOP include difficulties in recruitment due to the rarity of FOP, disease variability, the absence of reliable biomarkers, and ethical considerations regarding placebo-controlled trials. This narrative review provides an overview of the disease and explores emerging strategies for FOP treatment. Gene therapy, particularly the CRISPR-Cas9 (clustered regularly interspaced short palindromic repeats-associated protein 9) system, holds promise in treating FOP by specifically targeting the ACVR1 gene mutation. Another gene therapy approach being investigated is RNA interference, which aims to silence the mutant ACVR1 gene. Small molecule inhibitors targeting glycogen synthase kinase-3ß and modulation of the bone morphogenetic protein signaling pathway are also being explored as potential therapies for FOP. Stem cell-based approaches, such as mesenchymal stem cells and induced pluripotent stem cells, show potential in tissue regeneration and inhibiting abnormal bone formation in FOP. Immunotherapy and nanoparticle delivery systems provide alternative avenues for FOP treatment.