Key result
AT(2) gene deletion in mice significantly improved angiographic vessel density and laser Doppler perfusion in ischemic hindlimbs by 1.9- and 1.7-fold compared with wild-type controls.
Why the study?
Does AT2 receptor deletion improve angiogenesis in a mouse model of hindlimb ischemia?
Population
Wild-type and AT2 gene-deleted mice (Agtr2/Y) with surgically induced hindlimb ischemia via femoral artery…
Comparison
AT2 gene deletion (Agtr2/Y) and/or Angiotensin… vs Wild-type control mice
Design
Preclinical
Follow-up
28 days
Authors
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AT2 deletion improves angiogenesis in murine hindlimb ischemia; leaves open whether AT2 blockade aids human peripheral artery disease.
Does AT2 receptor deletion improve angiogenesis in a mouse model of hindlimb ischemia?
Effect estimate: 1.9- and 1.7-fold improvement
The AT2 receptor subtype negatively modulates ischemia-induced angiogenesis through activation of the apoptotic process in a mouse model of hindlimb ischemia.
Silvestre et al. (2002) studied Surgically induced hindlimb ischemia. AT(2) gene deletion (Agtr2(-)/Y) vs. Wild-type controls was evaluated on Angiogenesis (angiographic vessel density and laser Doppler perfusion) (1.9- and 1.7-fold improvement). AT(2) gene deletion in mice significantly improved angiographic vessel density and laser Doppler perfusion in ischemic hindlimbs by 1.9- and 1.7-fold compared with wild-type controls.
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