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. 2016 Jun 30;5(7):e003730. doi: 10.1161/JAHA.116.003730

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© 2016 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.

This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

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Hypothesis concerning cytokine‐induced hypertension. A model of hypertension involving LIGHT (an acronym for homologous to lymphotoxins, exhibits Inducible expression, and competes with herpes simplex virus glycoprotein D for herpes virus entry mediator, a receptor expressed by T lymphocytes, also known as TNFSF14) induced tissue transglutaminase (TG2) and the posttranslational modification (PTM) of AT₁ angiotensin receptor (AT₁Rs) resulting in the creation of a neoantigen that underlies autoimmune production of agonistic autoantibodies to the AT₁ angiotensin receptor (AT₁‐AAs). The resulting autoantibodies contribute to hypertension by activation of AT ₁Rs.