High molecular weight kininogen contributes to early mortality and kidney dysfunction in a mouse model of sickle cell disease.

ABSTRACT:

Background

Sickle cell disease (SCD) is characterized by chronic hemolytic anemia, vaso-occlusive crises, chronic inflammation, and activation of coagulation. The clinical complications such as painful crisis, stroke, pulmonary hypertension, nephropathy and venous thromboembolism lead to cumulative organ damage and premature death. High molecular weight kininogen (HK) is a central cofactor for the kallikrein-kinin and intrinsic coagulation pathways, which contributes to both coagulation and inflammation.

Objective

We hypothesize that HK contributes to the hypercoagulable and pro-inflammatory state that causes end-organ damage and early mortality in sickle mice.

Methods

We evaluated the role of HK in the Townes mouse model of SCD.

Results/conclusions

We found el

SUBMITTER: Sparkenbaugh EM 

PROVIDER: S-EPMC8043232 | biostudies-literature | 2020 Sep

REPOSITORIES: biostudies-literature