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Role of hepcidin‐ferroportin axis in the pathophysiology, diagnosis, and treatment of anemia of chronic inflammation
Author(s) -
Langer Arielle L.,
Ginzburg Yelena Z.
Publication year - 2017
Publication title -
hemodialysis international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.658
H-Index - 47
eISSN - 1542-4758
pISSN - 1492-7535
DOI - 10.1111/hdi.12543
Subject(s) - hepcidin , ferroportin , erythropoiesis , medicine , inflammation , anemia , pathophysiology , ineffective erythropoiesis , immunology , anemia of chronic disease , immune system
Anemia of chronic inflammation (ACI) is a frequently diagnosed anemia and portends an independently increased morbidity and poor outcome associated with multiple underlying diseases. The pathophysiology of ACI is multifactorial, resulting from the effects of inflammatory cytokines which both directly and indirectly suppress erythropoiesis. Recent advances in molecular understanding of iron metabolism provide strong evidence that immune mediators, such as IL‐6, lead to hepcidin‐induced hypoferremia, iron sequestration, and decreased iron availability for erythropoiesis. The role of hepcidin‐ferroportin axis in the pathophysiology of ACI is stimulating the development of new diagnostics and targeted therapies. In this review, we present an overview of and rationale for inflammation‐, iron‐, and erythropoiesis‐related strategies currently in development.