The prevalence of type 2 diabetes mellitus (T2DM) has quadrupled within three decades
since 1980, affecting 422 million adults in 2016. It remains one of the most common noncommunicable
chronic diseases and the underlying risk factor for cardiovascular diseases worldwide.
There are different underlying mechanisms that play a role in the development of pathologies associated
with the disease such as hyperglycaemia, oxidative stress, obesity, inflammation and hypercoagulation;
each of which are interlinked. Hyperglycaemia, oxidative stress and obesity play a huge role in
the activation of inflammation and coagulation. Activation of inflammatory pathways increases the
production of thrombin which predisposes the development of thrombotic related diseases. One of the
factors that contribute to the increase of thrombin is the impairment of the fibrinolysis process due to
decreased expression of tissue-plasminogen activator (tPA) by increased levels of plasminogen activator
inhibitor-1 (PAI-1). Coagulation factor XIII (FXIII), a transglutaminase that is composed of
subunits A and B (FXIII-A2B2), is essential for the last step of fibrin clot formation in the coagulation
pathway. Genetic variation of FXIII-A in the form of single nucleotide polymorphisms (SNPs) alters
the activity of FXIII, altering clot properties which influence disease outcomes. This review discusses
the link between underlying mechanisms of T2DM, well known FXIII-A variants and coagulation.
Associations between single-nucleotide polymorphisms (+45T>G, +276G>T, −11377C>G, −11391G>A) of adiponectin gene and type 2 diabetes mellitus: a systematic review and meta-analysis
