ACKR2


ACKR2: A Receptor with Diverse Roles in Health and Disease

Description

ACKR2 (Atypical Chemokine Receptor 2), also known as CXCR7, is a G protein-coupled receptor (GPCR) that plays a crucial role in various biological processes. Unlike typical chemokine receptors, ACKR2 does not trigger intracellular signaling upon ligand binding, instead acting as a scavenger receptor for chemokines.

ACKR2 has a broad ligand specificity, binding to a wide range of chemokines, including CXCL1, CXCL2, CXCL5, and CXCL8. This unique ability enables ACKR2 to regulate chemokine levels, preventing excessive inflammation and maintaining tissue homeostasis.

Associated Diseases

Dysregulation of ACKR2 function has been linked to several diseases, including:

  • Cancer: ACKR2 overexpression is associated with tumor growth, metastasis, and resistance to therapy. In various cancer types, ACKR2 promotes cell proliferation, angiogenesis, and immune evasion.
  • Cardiovascular disease: ACKR2 deficiency has been implicated in the development of atherosclerosis, heart failure, and myocardial infarction. It reduces inflammation and promotes tissue repair.
  • Inflammatory bowel disease (IBD): ACKR2 plays a protective role in IBD by dampening inflammation and maintaining intestinal barrier integrity.
  • Asthma: ACKR2 has been shown to modulate airway inflammation and bronchoconstriction, suggesting its potential role in asthma therapy.

Did you Know ?

In a study involving over 1,000 cancer patients, researchers found that high ACKR2 expression was associated with a significantly worse prognosis and reduced survival rates. This highlights the potential importance of ACKR2 as a therapeutic target in cancer.



Disclaimer: The information provided here is not exhaustive by any means. Always consult your doctor or other qualified healthcare provider with any questions you may have regarding a medical condition, procedure, or treatment, whether it is a prescription medication, over-the-counter drug, vitamin, supplement, or herbal alternative.