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Annexin-A1 deficiency exacerbates pathological remodelling of the mesenteric vasculature in insulin-resistant, but not insulin-deficient, mice.


ABSTRACT:

Background and purpose

Arterial stiffness, a characteristic feature of diabetes, increases the risk of cardiovascular complications. Potential mechanisms that promote arterial stiffness in diabetes include oxidative stress, glycation and inflammation. The anti-inflammatory protein annexin-A1 has cardioprotective properties, particularly in the context of ischaemia. However, the role of endogenous annexin-A1 in the vasculature in both normal physiology and pathophysiology remains largely unknown. Hence, this study investigated the role of endogenous annexin-A1 in diabetes-induced remodelling of mouse mesenteric vasculature.

Experimental approach

Insulin-resistance was induced in male mice (AnxA1+/+ and AnxA1-/- ) with the combination of streptozotocin (5

SUBMITTER: Jelinic M 

PROVIDER: S-EPMC7060371 | biostudies-literature | 2020 Apr

REPOSITORIES: biostudies-literature