CCL24 and Fibrosis: A Narrative Review of Existing Evidence and Mechanisms

Tissue fibrosis results from a dysregulated and chronic wound healing response accompanied by chronic inflammation and angiogenesis. Regardless of the affected organ, fibrosis shares the following common hallmarks: the recruitment of immune cells, fibroblast activation/proliferation, and excessive e...

Full description

Saved in:
Bibliographic Details
Main Authors: Raanan Greenman, Chris J. Weston
Format: Article
Language:English
Published: MDPI AG 2025-01-01
Series:Cells
Subjects:
Online Access:https://www.mdpi.com/2073-4409/14/2/105
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1832588837345296384
author Raanan Greenman
Chris J. Weston
author_facet Raanan Greenman
Chris J. Weston
author_sort Raanan Greenman
collection DOAJ
description Tissue fibrosis results from a dysregulated and chronic wound healing response accompanied by chronic inflammation and angiogenesis. Regardless of the affected organ, fibrosis shares the following common hallmarks: the recruitment of immune cells, fibroblast activation/proliferation, and excessive extracellular matrix deposition. Chemokines play a pivotal role in initiating and advancing these fibrotic processes. CCL24 (eotaxin-2) is a chemokine secreted by immune cells and epithelial cells, which promotes the trafficking of immune cells and the activation of profibrotic cells through CCR3 receptor binding. Higher levels of CCL24 and CCR3 were found in the tissue and sera of patients with fibro-inflammatory diseases, including primary sclerosing cholangitis (PSC), systemic sclerosis (SSc), and metabolic dysfunction-associated steatohepatitis (MASH). This review delves into the intricate role of CCL24 in fibrotic diseases, highlighting its impact on fibrotic, immune, and vascular pathways. We focus on the preclinical and clinical evidence supporting the therapeutic potential of blocking CCL24 in diseases that involve excessive inflammation and fibrosis.
format Article
id doaj-art-5bfea6307b6f44c1abfae16b2236a509
institution Kabale University
issn 2073-4409
language English
publishDate 2025-01-01
publisher MDPI AG
record_format Article
series Cells
spelling doaj-art-5bfea6307b6f44c1abfae16b2236a5092025-01-24T13:26:41ZengMDPI AGCells2073-44092025-01-0114210510.3390/cells14020105CCL24 and Fibrosis: A Narrative Review of Existing Evidence and MechanismsRaanan Greenman0Chris J. Weston1Chemomab Therapeutics Ltd., Tel Aviv 6158002, IsraelDepartment of Immunology and Immunotherapy, School of Infection, Inflammation and Immunology, College of Medicine and Health, University of Birmingham, Birmingham B15 2TT, UKTissue fibrosis results from a dysregulated and chronic wound healing response accompanied by chronic inflammation and angiogenesis. Regardless of the affected organ, fibrosis shares the following common hallmarks: the recruitment of immune cells, fibroblast activation/proliferation, and excessive extracellular matrix deposition. Chemokines play a pivotal role in initiating and advancing these fibrotic processes. CCL24 (eotaxin-2) is a chemokine secreted by immune cells and epithelial cells, which promotes the trafficking of immune cells and the activation of profibrotic cells through CCR3 receptor binding. Higher levels of CCL24 and CCR3 were found in the tissue and sera of patients with fibro-inflammatory diseases, including primary sclerosing cholangitis (PSC), systemic sclerosis (SSc), and metabolic dysfunction-associated steatohepatitis (MASH). This review delves into the intricate role of CCL24 in fibrotic diseases, highlighting its impact on fibrotic, immune, and vascular pathways. We focus on the preclinical and clinical evidence supporting the therapeutic potential of blocking CCL24 in diseases that involve excessive inflammation and fibrosis.https://www.mdpi.com/2073-4409/14/2/105CCL24CCR3chemokineeotaxin-2fibrosissystemic sclerosis
spellingShingle Raanan Greenman
Chris J. Weston
CCL24 and Fibrosis: A Narrative Review of Existing Evidence and Mechanisms
Cells
CCL24
CCR3
chemokine
eotaxin-2
fibrosis
systemic sclerosis
title CCL24 and Fibrosis: A Narrative Review of Existing Evidence and Mechanisms
title_full CCL24 and Fibrosis: A Narrative Review of Existing Evidence and Mechanisms
title_fullStr CCL24 and Fibrosis: A Narrative Review of Existing Evidence and Mechanisms
title_full_unstemmed CCL24 and Fibrosis: A Narrative Review of Existing Evidence and Mechanisms
title_short CCL24 and Fibrosis: A Narrative Review of Existing Evidence and Mechanisms
title_sort ccl24 and fibrosis a narrative review of existing evidence and mechanisms
topic CCL24
CCR3
chemokine
eotaxin-2
fibrosis
systemic sclerosis
url https://www.mdpi.com/2073-4409/14/2/105
work_keys_str_mv AT raanangreenman ccl24andfibrosisanarrativereviewofexistingevidenceandmechanisms
AT chrisjweston ccl24andfibrosisanarrativereviewofexistingevidenceandmechanisms