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. Author manuscript; available in PMC: 2022 Jul 21.
Published in final edited form as: Cell Mol Life Sci. 2021 Feb 11;78(9):4161–4187. doi: 10.1007/s00018-021-03779-w

Figure 3. The potential molecular mechanism by which Angiotensin II signaling via ADAM17 mediates chronic vascular pathology in hypertension,

Figure 3.

Angiotensin II rapidly activates ADAM17 via its Tyr702 phosphorylation through the GPCR, AT1 receptor (AT1R) in VSMCs. This leads to proHB-EGF shedding and subsequent EGFR transactivation. Enhanced protein synthesis results in protein misfolding causing protein aggregate formation. Protein aggregates prolong ER stress and UPR which transcriptionally upregulate ADAM17 thus create the feed-forward loop of sustained signaling leading to hypertensive vascular remodeling.