Abstract

Uterine fibroids are highly prevalent understudied myometrial non-cancerous tumors of the female reproductive tract. Fibroids cause increased morbidity and a significant economic burden in women. Despite its high prevalence, the only gold standard treatment for fibroid is hysterectomy. The tumor masses of fibroids are predominantly composed of excessive extracellular matrix when compared to the aberrant tumour cell population. The apoptotic resistance of matrix secreting cells during chronic inflammatory state such as fibroids, leads to deposition of enhanced rigid matrix molecules that are both responsible for tumour cell proliferation via the mechano-transduction process and the manifestation of bulk symptoms such as pain and bleeding. Despite its established fibrotic background and resemblances to pathological fibrosis most of the drugs are introduced as anti-proliferative and not as anti-fibrotic. This review aims in understanding the fibrotic mechanisms associated with the disease and emphasizes on drugs decreasing matrix production and increasing matrix dissolution. Such a modulation could bypass adverse effects associated with current pharmacological interventions that exert its therapeutic effect by modulation of hormones.