Targeting fibrosis, mechanisms and cilinical trials

Area of Science:

• Fibrosis research
• Cellular biology
• Pathology

Background:

• Fibrosis is excessive extracellular matrix deposition from dysregulated tissue repair.
• It affects multiple organs, including liver, kidney, heart, and lung, causing significant disease burden.
• Persistent myofibroblast activation, driven by signals like TGF-β, is central to fibrosis progression.

Purpose of the Study:

• To review the etiology, epidemiology, and mechanisms of major fibrotic diseases.
• To summarize cellular players and aberrant signaling pathways in fibrosis.
• To discuss current and emerging anti-fibrotic therapeutic targets and drugs.

Main Methods:

• Literature review of fibrosis mechanisms, cell interactions, and signaling pathways.
• Analysis of therapeutic targets and clinical trial data for anti-fibrotic drugs.
• Synthesis of information on organ-specific fibrosis, including liver, kidney, cardiac, and pulmonary fibrosis.

Main Results:

• Identified key abnormal cells (epithelial, endothelial, immune, fibroblasts) and their interactions in fibrosis.
• Detailed aberrant signaling pathways regulating myofibroblast activation, ECM cross-linking, metabolism, and inflammation.
• Highlighted drugs targeting these pathways showing efficacy in clinical trials.

Conclusions:

• Understanding fibrosis mechanisms is crucial for developing effective treatments.
• Targeting specific signaling pathways and cellular interactions offers promising anti-fibrotic strategies.
• This review provides a foundation for future fibrosis research, drug development, and clinical trials.