Elimination of fibrin polymer formation or crosslinking, but not fibrinogen deficiency, is protective against diet-induced obesity and associated pathologies.

ABSTRACT:

Background

Obesity predisposes individuals to metabolic syndrome, which increases the risk of cardiovascular diseases, non-alcoholic fatty liver disease (NAFLD), and type 2 diabetes. A pathological manifestation of obesity is the activation of the coagulation system. In turn, extravascular fibrin(ogen) deposits accumulate in adipose tissues and liver. These deposits promote adiposity and downstream sequelae by driving pro-inflammatory macrophage function through binding the leukocyte integrin receptor α_M β₂ .

Objectives

An unresolved question is whether conversion of soluble fibrinogen to a crosslinked fibrin matrix is required to exacerbate obesity-driven diseases.

Methods

Here, fibrinogen-deficient/depleted mice (Fib- or treated with siRNA agai

SUBMITTER: Hur WS 

PROVIDER: S-EPMC9669152 | biostudies-literature | 2022 Dec

REPOSITORIES: biostudies-literature