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Linking Inflammation and Hypertension via LNK/SH2B3 #MMPMID26717315
Dale BL; Madhur MS
Curr Opin Nephrol Hypertens 2016[Mar]; 25 (2): 87-93 PMID26717315show ga
Purpose of review: Hypertension is a leading cause of cardiovascular and renal morbidity and mortality. Genome wide association studies identified a single nucleotide polymorphism in the gene SH2B3 encoding the lymphocyte adaptor protein, LNK, but until recently, little was known about how LNK contributes to hypertension. This review summarizes recent work highlighting a central role for LNK in inflammation and hypertension. Recent findings: Using a systems biology approach that integrates genomic data with whole blood transcriptomic data and network modeling, LNK/SH2B3 was identified as a key driver gene for hypertension in humans. LNK is an intracellular adaptor protein expressed predominantly in hematopoietic and endothelial cells that negatively regulates cell proliferation and cytokine signaling. Genetic animal models with deletion or mutation of LNK revealed an important role for LNK in renal and vascular inflammation, glomerular injury, oxidative stress, interferon gamma (IFN?) production, and hypertension. Bone marrow transplantation experiments revealed that LNK in hematopoietic cells is primarily responsible for blood pressure regulation. Summary: LNK/SH2B3 is a key driver gene for human hypertension, and alteration of LNK in animal models has a profound effect on inflammation and hypertension. Thus, LNK is a potential therapeutic target for this disease and its devastating consequences.