Exploring New Therapeutic Targets for the Treatment of Large Vessel Vasculitis

Melissa Sharon^*
*Correspondence: Melissa Sharon, Department of Vasculitis, University of Oregon, 1585 E 13 Ave, Eugene, OR 97403, USA, Email:

Keywords

Vasculitis • Therapeutic • Studies

Introduction

Large Vessel Vasculitis (LVV) encompasses a spectrum of autoimmune disorders characterized by inflammation of the aorta and its major branches. Giant Cell Arteritis (GCA) and Takayasu Arteritis (TA) are the two most common forms of LVV, presenting with distinct clinical features and disease manifestations. Despite advancements in treatment, challenges remain in achieving sustained remission, minimizing glucocorticoid exposure, and managing treatment-related adverse effects. This article explores new therapeutic targets and emerging treatment strategies for LVV, aiming to improve outcomes and quality of life for affected patients [1].

Literature Review

The pathogenesis of LVV involves complex interactions between innate and adaptive immune responses, endothelial dysfunction, and vascular remodeling processes. Dysregulated immune activation leads to infiltration of inflammatory cells into the vessel wall, disruption of vascular integrity, and subsequent tissue damage. Key cytokines, chemokines, and immune pathways implicated in LVV pathogenesis Include Interleukin-6 (IL-6), Tumor Necrosis Factor-Alpha (TNF-alpha), and Janus Kinase (JAK)-Signal Transducer and Activator of Transcription (STAT) signaling. Agents targeting the IL-6 pathway, such as tocilizumab, have shown efficacy in GCA by reducing acute-phase reactants, improving symptoms, and minimizing glucocorticoid exposure [2].

Discussion

Ongoing research is investigating the long-term safety and durability of response to IL-6 inhibition in GCA. TNF-alpha inhibitors, including infliximab and adalimumab, have demonstrated efficacy in refractory cases of GCA and TA. These agents modulate immune responses and reduce vascular inflammation, offering an alternative treatment option for patients with glucocorticoidresistant disease. JAK inhibitors, such as tofacitinib and baricitinib, target the JAK-STAT signaling pathway involved in immune cell activation and cytokine production. Early studies suggest potential efficacy of JAK inhibition in LVV, although further research is needed to confirm these findings and evaluate long-term safety [3-5].

Combining immunomodulatory agents with different mechanisms of action, such as IL-6 inhibitors with TNF-alpha inhibitors or JAK inhibitors, may enhance treatment efficacy and minimize glucocorticoid exposure in LVV. Clinical trials evaluating combination therapy approaches are underway to assess safety and efficacy outcomes. Emerging research focuses on targeting vascular remodeling processes, including endothelial dysfunction, smooth muscle cell proliferation, and angiogenesis, to mitigate vessel wall damage and promote vascular healing in LVV. Small molecule inhibitors, growth factor antagonists, and angiogenesis inhibitors are being investigated as potential therapeutic agents in preclinical and clinical studies [6,7].

Conclusion

Large vessel vasculitis represents a challenging autoimmune condition characterized by inflammation of the aorta and its major branches. Despite advancements in treatment, achieving sustained remission and minimizing treatment-related adverse effects remain significant challenges. By exploring novel therapeutic targets and emerging treatment strategies, healthcare providers can optimize outcomes and improve quality of life for patients with LVV. Ongoing research efforts aimed at elucidating the underlying pathophysiological mechanisms and investigating innovative treatment approaches hold promise for advancing the field of LVV management and addressing unmet clinical needs.

Acknowledgement

None.

Conflict of Interest

None.

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