Application of GLP-1R nuclear export in regulating vascular remodeling
By elucidating the molecular mechanism of GLP-1R nuclear output, and utilizing the AngII→AT1R→PI3K/PDK1/Akt→PKCθ→GLP-1R Ser416 phosphorylation signaling pathway, a new strategy for inhibiting vascular remodeling was provided, solving the problem of drug targets and diagnostic methods for vascular remodeling-related cardiovascular diseases, and realizing the regulation of vascular smooth muscle cell function.
Patent Information
- Authority / Receiving Office
- CN · China
- Patent Type
- Applications(China)
- Current Assignee / Owner
- TAIYUAN NORMAL UNIV
- Filing Date
- 2026-04-21
- Publication Date
- 2026-07-17
AI Technical Summary
Current technologies have failed to clarify the molecular mechanism of GLP-1R nuclear output under pathological conditions of vascular remodeling, and lack effective drug targets and intervention strategies to inhibit the abnormal proliferation and migration of vascular smooth muscle cells, leading to the progression of cardiovascular disease.
This study elucidates that GLP-1R nuclear output is induced by AngII, and that the signaling pathway involves AngII→AT1R→PI3K/PDK1/Akt→PKCθ→GLP-1R Ser416 phosphorylation. By using substances such as PKCθ inhibitors and GLP-1R Ser416 phosphorylation blockers, GLP-1R nuclear output can be inhibited, thereby blocking the process of vascular remodeling.
It provides new drug targets and treatment strategies that can effectively inhibit vascular remodeling-related diseases, including hypertension, atherosclerosis, restenosis after angioplasty, heart failure, diabetic vascular disease, and pulmonary hypertension, and uses the GLP-1R nucleocytoplasmic localization ratio as a biomarker for diagnosis and efficacy monitoring.
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