New paper: The role of reactive oxygen species in liver fibrosis and immune modulation

NN researcher Muling Zeng has published a new article in the journal Redox Biology. The study has been carried out in a collaboration network with de Shenzhen Longgang Second People's Hospital, Premium Research SL, IBIDAPS, University of Barcelona, and the CIBER EHD.

This review examines how ROS function as both signalling molecules and stress inducers, shaping macrophage activity and influencing the development and resolution of fibrosis. Understanding these interactions opens the door to personalised treatments that target ROS and immune cell reprogramming.

Title

Beyond M1/M2: The role of reactive oxygen species in liver fibrosis and immune modulation

DOI: 10.1016/j.redox.2025.103933

Abstract

Liver fibrosis is a progressive condition resulting from chronic liver injury and characterized by excessive extracellular matrix deposition and architectural disruption. Reactive oxygen species (ROS), long considered merely cytotoxic, are now recognized as key modulators of immune responses and fibrogenic pathways. In this context, macrophages play a central role. Traditionally classified into M1 (pro-inflammatory) and M2 (anti-inflammatory) phenotypes, macrophages exhibit greater heterogeneity and plasticity than this binary model suggests. This review critically re-evaluates the role of ROS in liver fibrosis, with emphasis on their dual functions as signaling mediators and inducers of oxidative stress. Particular attention is given to how ROS influence macrophage polarization, activation, and function within the fibrotic liver microenvironment, and how this crosstalk contributes to both fibrogenesis and resolution. By addressing the complexity of redox-immunological interactions, new opportunities emerge for more effective and personalized antifibrotic interventions, including targeted modulation of ROS and immune cell reprogramming. This integrative perspective will help guide the development of more effective and personalized antifibrotic treatments.