Key result
Adiponectin and AdipoRon attenuate Angiotensin II-induced vascular remodeling and smooth muscle cell migration.
Why the study?
The endogenous adiponectin and its receptor expression in perivascular adipocytes and their role in hypertensive vascular injury remain unclear.
p-value: p=<0.05
Perivascular adipocyte-derived adiponectin attenuates hypertensive vascular injury, suggesting a potential therapeutic target for hypertensive vascular disease.
APN expression in perivascular adipocytes may mitigate hypertensive vascular injury; leaves open therapeutic targeting pending clinical validation.
Adipocyte-derived adiponectin (APN) is involved in the protection against cardiovascular disease, but the endogenous APN and its receptor expression in the perivascular adipocytes and their role in hypertensive vascular injury remain unclear. The present study aimed to detect endogenous APN and its receptor expression and their protective effects against hypertensive vascular injury. APN was mainly expressed in the perivascular adipocytes, while its receptors AdipoR1 and AdipoR2 were ubiquitously expressed in the blood vessels. Angiotensin II (Ang II)‑induced hypertension resulted in a significant decrease of APN and AdipoR1 and AdipoR2 in the perivascular adipocytes and vascular cells. The migration assay used demonstrated that APN attenuated Ang II‑induced vascular smooth muscle cells migration and p38 phosphorylation Furthermore, the in vivo study demonstrated that APN receptor agonist AdipoRon attenuated Ang II‑induced hypertensive vascular hypertrophy and fibrosis. Taken together, the present study indicated that perivascular adipocytes‑derived APN attenuated hypertensive vascular injury possibly via its receptor‑mediated inhibition of p38 signaling pathway.
No takes yet. Share an insight, caveat, or question.
Guo et al. (2017) studied Hypertensive vascular injury (n=15). Adiponectin and AdipoRon vs. Angiotensin II alone or Sham was evaluated on Vascular hypertrophy, fibrosis, and vascular smooth muscle cell migration (p=<0.05). Adiponectin and the adiponectin receptor agonist AdipoRon significantly attenuated Angiotensin II-induced vascular smooth muscle cell migration, p38 phosphorylation, and hypertensive vascular remodeling.