Key result
Angiotensin II induces HDAC5 phosphorylation and nuclear export via the PI3K/Akt pathway, which regulates Egr-1 expression and cell hypertrophy in vascular smooth muscle cells.
This preclinical study elucidates the molecular mechanism by which Angiotensin II induces vascular smooth muscle cell hypertrophy via the Akt/HDAC5/Egr-1 pathway.
Preclinical VSMC pathway mapping leaves open translation to vascular disease therapies; in vivo and human studies needed before clinical consideration.
ANG II-induced histone deacetylase 5 (HDAC5) phosphorylation and nuclear export occurs via the phosphoinositide 3-kinase/Akt pathway. Akt, through HDAC5, regulates ANG II-induced expression of early growth response protein-1 (Egr-1), which is a transcription factor linked with vascular dysfunction. Inhibition of HDAC5 exclusion by nuclear export inhibitors suppresses ANG II-induced Egr-1 expression. HDAC5 is an upstream mediator of Egr-1 expression and cell hypertrophy in response to ANG II in vascular smooth muscle cells.
No takes yet. Share an insight, caveat, or question.
Truong et al. (2021) studied this question. Angiotensin II was evaluated on HDAC5 phosphorylation, nuclear export, and Egr-1 expression. Angiotensin II induces HDAC5 phosphorylation and nuclear export via the PI3K/Akt pathway, which regulates Egr-1 expression and cell hypertrophy in vascular smooth muscle cells.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: