Pentraxin 3 – a potential link between inflammation, obesity and cardiovascular complications in polycystic ovary syndrome

Abstract

Polycystic ovary syndrome (PCOS) is the most frequently diagnosed endocrine disorder among women in reproductive age. Metabolic disturbances in PCOS include among others increased incidence of insulin resistance and hyperinsulinemia, type 2 diabetes, dyslipidemia, pre-thrombotic state, hypertension, sleep apnea, atherosclerosis and cardiovascular diseases. Adipose tissue disturbances, including inflammation, were shown to play an important role in the development of both endocrine and metabolic disturbances, accelerating the progression of arteriosclerosis, which leads to premature cardiovascular disease development in PCOS. Pentraxin 3 (PTX3) seems to be one of the factors linking obesity and cardiovascular complications observed in PCOS. PTX3 belongs to a family of long pentraxin proteins. It primarily plays a role in acute immunological response; however, some data suggests that it may also be involved in oocyte maturation. In contrast to the short pentraxin, C-reactive protein, which is primarily produced in the liver, PTX3 is produced locally in the site of the inflammation by several types of cells, for example, adipose tissue during development of inflammation. Increased PTX3 expression was found in visceral fat tissue in obese subjects, and was shown to be under TNF-α control. PTX3 expression has not been tested in PCOS women, yet. Up to now there are only 5 studies investigating PTX3 in PCOS. Only in one study PTX3 level in PCOS women was increased compared to the control groups, in two other studies – decreased, and in two – similar. Also, the association between PTX3, PCOS and obesity remains uncertain. Further research, including ones with a greater number of subjects, especially obese and older women, are necessary to assess the role of PTX3 as a potential link between the inflammation, obesity and polycystic ovary syndrome.