Isshiki, Takuma, Vierhout, Megan, Naiel, Safaa, Ali, Pareesa, Yazdanshenas, Parichehr, Kumaran, Vaishnavi, Yang, Zi, Dvorkin-Gheva, Anna, Rullo, Anthony F, Kolb, Martin R J and Ask, Kjetil (2023) Therapeutic strategies targeting pro-fibrotic macrophages in interstitial lung disease. Biochemical pharmacology, 211. p. 115501. ISSN 1873-2968

Abstract

Idiopathic pulmonary fibrosis (IPF) is the representative phenotype of interstitial lung disease where severe scarring develops in the lung interstitium. Although antifibrotic treatments are available and have been shown to slow the progression of IPF, improved therapeutic options are still needed. Recent data indicate that macrophages play essential pro-fibrotic roles in the pathogenesis of pulmonary fibrosis. Historically, macrophages have been classified into two functional subtypes, "M1″ and "M2," and it is well described that "M2″ or "alternatively activated" macrophages contribute to fibrosis via the production of fibrotic mediators, such as TGF-β, CTGF, and CCL18. However, highly plastic macrophages may possess distinct functions and phenotypes in the fibrotic lung environment. Thus, M2-like macrophages in vitro and pro-fibrotic macrophages in vivo are not completely identical cell populations. Recent developments in transcriptome analysis, including single-cell RNA sequencing, have attempted to depict

Item Type:	Article
Date Deposited:	28 Dec 2024 00:45
Last Modified:	28 Dec 2024 00:45
URI:	https://oak.novartis.com/id/eprint/56175