The Roles of Various Prostaglandins in Fibrosis: A Review

Abstract

Organ fibrosis is a common pathological result of various chronic diseases with multiple causes. Fibrosis is characterized by the excessive deposition of extracellular matrix and eventually leads to the destruction of the tissue structure and impaired organ function. Prostaglandins are produced by arachidonic acid through cyclooxygenases and various prostaglandin-specific synthases. Prostaglandins bind to homologous receptors on adjacent tissue cells in an autocrine or paracrine manner and participate in the regulation of a series of physiological or pathological processes, including fibrosis. This review summarizes the properties, synthesis, and degradation of various prostaglandins, as well as the roles of these prostaglandins and their receptors in fibrosis in multiple models to reveal the clinical significance of prostaglandins and their receptors in the treatment of fibrosis.

Agonists of prostaglandin E 2 receptors as potential first in class treatment for nephronophthisis and related ciliopathies

“…In accordance with our results, EP2 and EP4 activation was described to exert antifibrotic properties in several models of kidney fibrosis ( 57 , 58 ), and was shown to play a major role in the differentiation of myofibroblasts and expression of extracellular matrix proteins ( 59 ). Altogether, our results suggest that the NPHP1 -deficient background (KO mice and URECs) is sensitive to PGE1 treatment, which, in addition to its positive effects on ciliogenesis, has a protective effect on profibrotic gene expression and renal lesions.…”

Differential Staining Patterns for Evaluation of Ovarian and Oviducts Fibrosis Using the Polarized Light Microscope and the Digital Images Analysis

“…The immunological environment within the lumen of the oviduct is maintained by the mucosal layer. Chronic inflammation can cause oviduct mucosal injury and immunological malfunction, causing infertility, early pregnancy abortion, ectopic pregnancy, and even tumors, in addition to diminished reproductive capacities [1] . Our results showed that HFD consumption induced fibrosis in ovary and oviduct, which represented by significant increase of hydroxyproline and collagen fibers (demonstrated via histological stains as MT, PSR, and VG) in addition to immunohistochemical overexpression of vimentin and α-SMA in both ovary and oviducts.…”

“…Fibrosis is commonly demonstrated in different organs as heart, kidney, lungs, liver, and testis. Without effective treatment, fibrosis impaired organ function and ultimately induces organ malfunction [1][2][3][4] . Fibrosis is characterized by excessive scaring formation instead of normal tissue, which then finally results in the destruction of the tissue architecture and organ remodeling.…”

“…Fibrosis is characterized by excessive scaring formation instead of normal tissue, which then finally results in the destruction of the tissue architecture and organ remodeling. Scaring is related to multiple causes including increased fibroblasts proliferation, excessive deposition of connective tissue components as extracellular matrix (ECM) proteins, with ECM development influenced by a number of molecular components including transforming growth factor-β (TGF-β), connective tissue growth factor, and epidermal growth factor [1,2,5] . Collagens, elastin, glycoproteins, and proteoglycans are the main components of ECM, which comprise connective tissues and basement membranes.…”

Pathogenic Mechanisms of Pulmonary Arterial Hypertension

“… 36 PGE 2 also plays an antifibrotic role, primarily through binding to PGE 2 receptors 2 and 4. 37 PGF 2α is a potent fibrosis factor, which is abundant in the lung bronchoalveolar lavage fluid of patients with idiopathic pulmonary fibrosis. 38 The fibrotic pathway activated by PGF 2α is thought to be independent of the transforming growth factor–β pathway in promoting fibrosis.…”