Mechanisms of fibrosis: therapeutic translation for fibrotic disease
Open accessAbstract
Fibrosis is a pathological feature of most chronic inflammatory diseases. Fibrosis, or scarring, is defined by the accumulation of excess extracellular matrix components. If highly progressive, the fibrotic process eventually leads to organ malfunction and death. Fibrosis affects nearly every tissue in the body. Here we discuss how key components of the innate and adaptive immune response contribute to the pathogenesis of fibrosis. We also describe how cell-intrinsic changes in important structural cells can perpetuate the fibrotic response by regulating the differentiation, recruitment, proliferation and activation of extracellular matrix-producing myofibroblasts. Finally, we highlight some of the key mechanisms and pathways of fibrosis that are being targeted as potential therapies for a variety of important human diseases.
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Several cell types contribute to liver fibrosis, including hepatic stellate cells (HSCs) and other fibroblasts, liver sinusoidal endothelial cells (LSECs), and hepatocytes; the immune system also plays key roles.
“Several cell types contribute to liver fibrosis, including hepatic stellate cells (HSCs) and other fibroblasts, liver sinusoidal endothelial cells (LSECs), and hepatocytes; however, the immune system also plays key roles (2, 6).”
From Targeting macrophages in liver fibrosis (2026) · cites this paper as [2]
The ‘Innate immunity and fibrosis’ sections identify hepatic stellate cells as liver fibroblasts and describe roles for macrophages and dendritic cells in liver fibrosis. The ‘Endoplasmic reticulum stress’ section links hepatocyte apoptosis to liver fibrosis in NASH. Our copy does not identify liver sinusoidal endothelial cells specifically as contributors, so the full cell-type list is not supported. (LLM, conf=0.84)
Experimental — accuracy not yet measuredFibrosis results from excessive deposition of extracellular matrix (ECM) components following tissue injury.
“Fibrosis results from excessive deposition of extracellular matrix (ECM) components following tissue injury.”
From Targeting macrophages in liver fibrosis (2026) · cites this paper as [2]
Proinflammatory cytokines from senescent cells, such as MCP-1, TNF-α, and IL-1β, are considered among the most important drivers of dysfunctional adipose tissue and chronic fibrotic disease.
“In contrast, the proinflammatory cytokines released from senescent cells, including MCP-1, TNF-α, and IL-1β, are among those considered most important for the progression to dysfunctional AT and chronic fibrotic disease (65,113).”
From The ominous triad of adipose tissue dysfunction: inflammation, fibrosis, and impaired angiogenesis. (2017) · cites this paper as [65]
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- Authors
- Wynn, T. A., & Ramalingam, T. R.
- Affiliations
- National Institutes of Health (US)
- Corresponding author
- Wynn, Thomas A
- Venue
- Nature Medicine
- Published
- 2012-07
- Volume
- 18
- Issue
- 7
- Pages
- 1028-1040
- ISSN
- 1078-8956 (ISSN-L)
- 1546-170X
- PMC
- PMC3405917
- OpenAlex
- W2045142779
- Cited by
- 3,541
- References
- 183
- Citations by year
- 2026: 294 · 2025: 333 · 2024: 299 · 2023: 322 · 2022: 288 · 2021: 332 · 2020: 301 · 2019: 254 · 2018: 247 · 2017: 228 · 2016: 182 · 2015: 180 · 2014: 151 · 2013: 108 · 2012: 15
- FWCI
- 24.72
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute of Allergy and Infectious Diseases (ZIAAI001019)
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Keywords
- fibrosis, chronic inflammation, innate immune response, adaptive immune response, extracellular matrix accumulation, myofibroblasts, fibroblast activation, fibrosis treatment
- MeSH terms
- Fibrosis, Humans, Immunity, Wound Healing, Inflammation Mediators, Translational Research, Biomedical, Myofibroblasts
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