Why the study?
Although Ang II stimulates ERK1/2 and VSMC proliferation, whether Ang III induces ERK1/2 MAPK and proliferation in Wistar and SHR VSMCs remained to be explored.
Does Angiotensin III induce ERK1/2 MAPK phosphorylation and cellular proliferation in rat vascular smooth muscle cells?
Population
Cultured VSMCs from Wistar rats and spontaneously hypertensive rats
Comparison
Ang III vs Ang II exposure in Wistar vs SHR VSMCs
Design
In vitro laboratory study
Key result
Angiotensin III stimulates ERK1/2 MAPK phosphorylation and DNA synthesis in vascular smooth muscle cells via AT1 receptors, though this effect is reduced in spontaneously hypertensive rats.
Authors
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Ang III-AT1-ERK1/2 signaling may drive VSMC growth; leaves open relevance to human hypertension.
Does Angiotensin III induce ERK1/2 MAPK phosphorylation and cellular proliferation in rat vascular smooth muscle cells?
Angiotensin III stimulates ERK1/2 MAPK and DNA synthesis in vascular smooth muscle cells via AT1 receptors, with reduced effects in spontaneously hypertensive rats compared to normotensive rats.
Alanazi et al. (2025) studied this question. Angiotensin III vs. Angiotensin II / SHR vs Wistar VSMCs was evaluated on ERK1/2 MAPK phosphorylation and DNA synthesis. Angiotensin III stimulates ERK1/2 MAPK phosphorylation and DNA synthesis in vascular smooth muscle cells via AT1 receptors, though this effect is reduced in spontaneously hypertensive rats.
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