Key Takeaways & Executive Findings
- •• Fibrosis is a dysregulated tissue repair process characterized by fibroblast proliferation and excessive extracellular matrix deposition, affecting multiple organs. • Key abnormal cells include fibroblasts, immune cells, epithelial cells, and endothelial cells; fibroblasts are central to fibrosis progression. • Major signaling pathways (TGF-β, Wnt/β-catenin, Notch, TLR4/MyD88/NF-κB, Hippo/YAP) and epigenetic modifications regulate fibrosis. • Anti-fibrotic strategies include pharmacological, cell-based, and gene therapies targeting these pathways and extracellular matrix remodeling.
Abstract
BACKGROUND: Fibrosis results from dysregulated tissue healing, characterized by abnormal proliferation of fibroblasts and excessive deposition of extracellular matrix, affecting nearly all organs including liver, kidney, heart, lung, and skin. OBJECTIVE: To summarize fibrosis-related diseases such as liver, kidney, cardiac, and pulmonary fibrosis, focusing on the major abnormal cells, signaling pathways, and therapeutic approaches. METHODS: PubMed and CNKI were searched using English terms "fibrosis, fibroblasts, fibrotic organs, extracellular matrix, tissue repair, inflammatory response" and Chinese equivalents. After screening according to inclusion and exclusion criteria, 200 articles were included for review. RESULTS AND CONCLUSION: Key abnormal cells in fibrosis include immune cells (macrophages, neutrophils, lymphocytes), fibroblasts, epithelial cells, and endothelial cells, with fibroblasts playing a central role. Major abnormal pathways include TGF-β, Wnt/β-catenin, Notch, TLR4/MyD88/NF-κB, and Hippo/YAP signaling, whose dysregulation drives fibrosis. Epigenetic modifications (DNA methylation, histone modification, non-coding RNA regulation) modulate fibrosis progression. Anti-fibrotic therapies include pharmacological, cellular, and gene-based approaches, targeting signaling pathways to inhibit persistent fibroblast activation or modulating extracellular matrix deposition to alleviate fibrosis and improve organ function.
1. Introduction
Fibrotic diseases are characterized by excessive production and remodeling of scar tissue, which can lead to organ failure and death [1]. Fibrosis is a dysregulated repair response to chronic injury, fundamentally involving excessive synthesis and abnormal deposition of extracellular matrix, resulting in structural damage and functional impairment of organs. Fibrosis can affect multiple organs, with extensive research on liver [2], kidney [3], lung [4], heart [5], and skin [6]. Although these organs differ in physiological function and structure, the fibrotic process exhibits significant commonalities in etiology, pathological manifestations, core mechanisms, and ultimate impact.
Persistent tissue injury and chronic inflammation are major causes of organ fibrosis. Regardless of the organ, repeated or chronic stimuli—such as chronic viral infections (e.g., viral hepatitis [7]), metabolic disorders (e.g., diabetic nephropathy [8]), or physical injury (e.g., skin wounds [9])—can induce local persistent inflammation and subsequent fibrosis.
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LI Feihong, WANG Linrong, CHENG Leping (2026). Role of fibrosis in tissue injury repair. Chinese Journal of Tissue Engineering Research. https://doi.org/10.12307/2026.21246
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Frequently Asked Questions
What is fibrosis?
Fibrosis is a pathological condition resulting from dysregulated tissue repair, characterized by abnormal proliferation of fibroblasts and excessive deposition of extracellular matrix, leading to organ dysfunction.
Which organs are commonly affected by fibrosis?
Fibrosis can affect virtually any organ, including the liver, kidney, heart, lung, and skin.
What are the key cellular and molecular mechanisms in fibrosis?
Key mechanisms involve abnormal activation of fibroblasts and other cells (immune, epithelial, endothelial), dysregulation of signaling pathways such as TGF-β, Wnt/β-catenin, Notch, TLR4/MyD88/NF-κB, and Hippo/YAP, and epigenetic modifications.
What therapeutic approaches are being explored for fibrosis?
Therapeutic strategies include pharmacological agents targeting specific pathways, cell-based therapies, and gene therapy, aiming to inhibit fibroblast activation or modulate extracellular matrix deposition.
Why is fibrosis important in tissue injury repair?
Fibrosis represents an aberrant healing response that can impair normal tissue function and lead to organ failure, making it a critical target for therapeutic intervention.
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