Key result
Deletion of IGFBP-1 inhibited endothelial regeneration following injury, while overexpression of IGFBP-1 stimulated hindlimb perfusion and angiogenesis in insulin-resistant male mice.
Why the study?
Human studies suggest low IGFBP-1 levels are permissive for diabetes and cardiovascular disease, but whether loss of IGFBP-1 plays a causal role in predisposing to cardiometabolic disease remained unknown.
Does loss or overexpression of IGFBP-1 alter metabolic and vascular pathophysiology in male mice?
Population
Male transgenic mice
Comparison
IGFBP-1 knockout vs wild-type and IGFBP-1 overexpressing mice under normal and high-fat diet
Design
Preclinical loss-of-function and gain-of-function animal study
Authors
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May identify IGFBP-1 as target for vascular repair in insulin resistance; leaves open human translation from animal data.
Does loss or overexpression of IGFBP-1 alter metabolic and vascular pathophysiology in male mice?
Increasing IGFBP-1 levels promotes neovascularization in response to ischemia in insulin-resistant models, suggesting a potential therapeutic target for cardiometabolic vascular complications.
Haywood et al. (2019) studied Cardiometabolic disease. IGFBP-1 knockout and overexpression vs. Wild-type mice was evaluated on Metabolic phenotype, endothelial regeneration, and angiogenesis. Deletion of IGFBP-1 inhibited endothelial regeneration following injury, while overexpression of IGFBP-1 stimulated hindlimb perfusion and angiogenesis in insulin-resistant male mice.
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