Why the study?
Hyperglycemia and angiotensin II promote vascular smooth muscle cell senescence, but potential cross-talk and the effects of AT2 receptor stimulation remained unclarified.
Does AT2 receptor stimulation with compound 21 inhibit vascular smooth muscle cell senescence induced by Angiotensin II and hyperglycemia in mouse aortic VSMCs?
Population
Aortic VSMCs from adult male mice
Comparison
Ang II and/or high glucose with or without C21, 3-MA, or rapamycin vs control
Design
Preclinical in vitro study
Authors
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AT2 agonism may attenuate VSMC senescence in this model; hypothesis-generating and leaves open human translation.
Does AT2 receptor stimulation with compound 21 inhibit vascular smooth muscle cell senescence induced by Angiotensin II and hyperglycemia in mouse aortic VSMCs?
AT2 receptor stimulation with compound 21 inhibits vascular smooth muscle cell senescence induced by the synergistic effects of Angiotensin II and hyperglycemia, partly through modulation of autophagy, oxidative stress, and the p21-pRb pathway.
Bai et al. (2022) studied this question.