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Related Concept Videos

Mechanism of Angiogenesis01:10

Mechanism of Angiogenesis

Blood vessel formation starts early during embryonic development, around day 7. In the extraembryonic yolk sac, mesodermal precursor cells called hemangioblast proliferate and differentiate into angioblast. Angioblasts express vascular endothelial growth factor receptor 2 or VEGFR2, which binds VEGF-A, a proangiogenic factor, guiding blood vessel formation. VEGF signaling promotes angioblasts to form a blood island in the developing embryo. Angioblasts further differentiate, giving rise to...
Vascular Spasm01:16

Vascular Spasm

The vascular phase, also known as vasospasm, is the initial stage of hemostasis, crucial for preventing excessive bleeding when a blood vessel is injured. After a vessel is cut, nerves in the damaged area trigger pain and other sensory impulses. Simultaneously, the smooth muscles in the vessel wall contract, resulting in a vascular spasm. This contraction reduces the vessel's diameter at the injury site, slowing or stopping blood loss through the vessel wall. Vascular spasms typically last for...

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Related Experiment Video

Updated: May 15, 2026

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ANCA vasculitis: what is in the pipeline.

Abbal Koirala1, Aditi Singh, Duvuru Geetha

  • 1Division of Nephrology, Johns Hopkins School of Medicine, Baltimore, Maryland, USA.

Current Opinion in Nephrology and Hypertension
|May 14, 2026
PubMed
Summary

Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is now understood as a complex immune disorder. Advances in understanding AAV are driving targeted, steroid-sparing treatments and personalized care for improved outcomes.

Keywords:
ANCA-associated vasculitiscyclophosphamideeosinophilic granulomatosis with polyangiitisglucocorticoidsgranulomatosis with polyangiitismicroscopic polyangiitisplasma exchangerituximab

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An Immunohistopathologic Study to Profile the Folate Receptor Beta Macrophage and Vascular Immune Microenvironment in Giant Cell Arteritis

Published on: February 8, 2019

Area of Science:

  • Immunology
  • Rheumatology
  • Internal Medicine

Background:

  • Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is increasingly recognized as a complex immune-mediated inflammatory disorder.
  • Recent advances in understanding ANCA specificity, complement activation, neutrophil extracellular trap formation, genetic susceptibility, and environmental triggers have reshaped disease concepts.

Purpose of the Study:

  • To review recent developments in the understanding and treatment of AAV.
  • To highlight how these advances are informing current treatment strategies, disease stratification, and drug development.

Main Methods:

  • Focused review of recent scientific literature and clinical trial data.
  • Analysis of emerging therapeutic targets and treatment modalities in AAV.

Main Results:

  • Treatment has shifted from conventional therapies to targeted, steroid-sparing approaches, with rituximab being central.
  • New therapies like avacopan, IL-5 blockade, next-generation anti-CD20 antibodies, CAR-T cell strategies, and complement-directed therapies are reducing glucocorticoid exposure and toxicity.
  • Emerging treatments target B-cell pathways, including BAFF/APRIL blockade and tyrosine kinase inhibitors.

Conclusions:

  • Improved biologic insights are enabling biomarker-driven classification and mechanism-based therapy selection in AAV.
  • These advances aim to reduce treatment-related morbidity, enhance remission durability, and support personalized clinical care and research.