Polycystic ovary syndrome (PCOS) is a frequent endocrine disease in women during the reproductive
period. It is considered a complex metabolic disorder with long-term metabolic, as well as reproductive
consequences. Main pathophysiological pathways are related to the increased androgen levels and insulin resistance.
Nowadays, genetic origins of PCOS are acknowledged, with numerous genes involved in the pathogenesis
of hyperandrogenemia, insulin resistance, inflammation, and disturbed folliculogenesis. Rotterdam diagnostic
criteria are most widely accepted and four PCOS phenotypes have been recognized. Metabolic abnormalities
are more common in phenotypes 1 and 2. Women with classic PCOS are more obese and typically have the central
type of obesity, more prevalently displaying dyslipidemia, insulin resistance, and metabolic syndrome that
could be associated with an increased risk of cardiovascular complications during life. Heterogeneity of phenotypes
demands an individualized approach in the treatment of women with PCOS. Metabolic therapies involve
a lifestyle intervention followed by the introduction of insulin sensitizers including metformin and inositols,
glucagon-like peptide 1 receptor agonists (GLP-1 RA), as recently sodium-glucose cotransporter-2 (SGLT2) inhibitors.
The addition of an insulin sensitizer to the standard infertility therapy such as clomiphene citrate improves
ovulation and pregnancy rates. Our current review analyzes the contemporary knowledge of PCOS etiology
and etiopathogenesis, its cardiometabolic risks and their outcomes, as well as therapeutic advances for women