Peptidylarginine deiminase 4 promotes age-related organ fibrosis
Open accessAbstract
Aging promotes inflammation, a process contributing to fibrosis and decline in organ function. The release of neutrophil extracellular traps (NETs [NETosis]), orchestrated by peptidylarginine deiminase 4 (PAD4), damages organs in acute inflammatory models. We determined that NETosis is more prevalent in aged mice and investigated the role of PAD4/NETs in age-related organ fibrosis. Reduction in fibrosis was seen in the hearts and lungs of aged PAD4−/− mice compared with wild-type (WT) mice. An increase in left ventricular interstitial collagen deposition and a decline in systolic and diastolic function were present only in WT mice, and not in PAD4−/− mice. In an experimental model of cardiac fibrosis, cardiac pressure overload induced NETosis and significant platelet recruitment in WT but not PAD4−/− myocardium. DNase 1 was given to assess the effects of extracellular chromatin. PAD4 deficiency or DNase 1 similarly protected hearts from fibrosis. We propose a role for NETs in cardiac fibrosis and conclude that PAD4 regulates age-related organ fibrosis and dysfunction.
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A previous study found that aged mice exhibited an increased propensity for NETosis compared to younger mice.
“A previous study found that aged mice exhibited an increased propensity for NETosis compared to younger mice.”
From Inflammation and aging: signaling pathways and intervention therapies (2023) · cites this paper as [270]
This heightened NETosis activity was associated with the activation of peptidylarginine deiminase 4 (PAD4), an enzyme involved in the formation of NETs.
“This heightened NETosis activity was associated with the activation of peptidylarginine deiminase 4 (PAD4), an enzyme involved in the formation of NETs.”
From Inflammation and aging: signaling pathways and intervention therapies (2023) · cites this paper as [270]
The excessive formation of NETs was implicated in the development of age-related organ fibrosis.
“The excessive formation of NETs, in turn, was implicated in the development of age-related organ fibrosis.270”
From Inflammation and aging: signaling pathways and intervention therapies (2023) · cites this paper as [270]
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Neutrophil extracellular traps in immunity and disease
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Inflammation and aging: signaling pathways and intervention therapies
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“The excessive formation of NETs, in turn, was implicated in the development of age-related organ fibrosis.(270) In conclusion, the process of aging can adversely affect the ability of neutrophils to undergo NETosis.”
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Self-citationInflammation, Infection and Venous Thromboembolism
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Electrospun fiber‐based immune engineering in regenerative medicine
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Self-citationExtracellular DNA traps in inflammation, injury and healing
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Self-citationNeutrophil extracellular traps promote fibrous vascular occlusions in chronic thrombosis
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JAK2V617F-Mediated Clonal Hematopoiesis Accelerates Pathological Remodeling in Murine Heart Failure
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Cardiovascular Disease, Aging, and Clonal Hematopoiesis
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The Pathophysiological Role of Neutrophil Extracellular Traps in Inflammatory Diseases
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Self-citationNeutrophils in aging and aging‐related pathologies
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PAD4 deficiency improves bleomycin-induced neutrophil extracellular traps and fibrosis in mouse lung
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Immunothrombosis and thromboinflammation in host defense and disease
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Self-citationCathelicidins prime platelets to mediate arterial thrombosis and tissue inflammation
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FOXO1/3: Potential suppressors of fibrosis
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Midkine drives cardiac inflammation by promoting neutrophil trafficking and NETosis in myocarditis
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Nuclear envelope rupture and NET formation is driven by PKCα‐mediated lamin B disassembly
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Neutrophil extracellular traps and fibrocytes in ST-segment elevation myocardial infarction
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Tissue-level inflammation and ventricular remodeling in hypertrophic cardiomyopathy
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Serum and Serum Albumin Inhibit in vitro Formation of Neutrophil Extracellular Traps (NETs)
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Insights into peptidylarginine deiminase expression and citrullination pathways
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Aging Reprograms the Hematopoietic-Vascular Niche to Impede Regeneration and Promote Fibrosis.
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CXCL4 drives fibrosis by promoting several key cellular and molecular processes
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HMGB1‐Promoted Neutrophil Extracellular Traps Contribute to Cardiac Diastolic Dysfunction in Mice
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Neutrophil inhibition improves acute inflammation in a murine model of viral myocarditis
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NETosis as a Pathogenic Factor for Heart Failure
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Upregulation of citrullination pathway: From Autoimmune to Idiopathic Lung Fibrosis
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Chemokines in cardiac fibrosis
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Neutrophils are indispensable for adverse cardiac remodeling in heart failure
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Von Willebrand factor exacerbates heart failure through formation of neutrophil extracellular traps
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Seipin Knockout Mice Develop Heart Failure With Preserved Ejection Fraction
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Leukocyte-Dependent Regulation of Cardiac Fibrosis
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Can we remove scar and fibrosis from adult human myocardium?
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The virtues and vices of protein citrullination
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Eosinophils in fungal diseases: An overview
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The role of NETosis in heart failure
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Identification of a Novel HIF-1α-αMβ2 Integrin-NET Axis in Fibrotic Interstitial Lung Disease
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The power from within – understanding the driving forces of neutrophil extracellular trap formation
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Self-citationCRP Induces NETosis in Heart Failure Patients with or without Diabetes
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Benzyl butyl phthalate (BBP) induces lung injury and fibrosis through neutrophil extracellular traps
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Neutrophil Extracellular Traps: Inflammation and Biomaterial Preconditioning for Tissue Engineering
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NETosis promotes chronic inflammation and fibrosis in systemic lupus erythematosus and COVID-19
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NLRP3-Induced NETosis: A Potential Therapeutic Target for Ischemic Thrombotic Diseases?
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Subclinical Inflammation in Heart Failure: A Neutrophil Perspective
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NADPH Oxidase Inhibition in Fibrotic Pathologies
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Externalized histones fuel pulmonary fibrosis via a platelet-macrophage circuit of TGFβ1 and IL-27
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- Authors
- Martinod, K., Witsch, T., Erpenbeck, L., Savchenko, A., Hayashi, H., Cherpokova, D., Gallant, M., Mauler, M., Cifuni, S. M., & Wagner, D. D.
- Affiliations
- Boston Children's Hospital (US)
- University of Freiburg (DE)
- Corresponding author
- Wagner, Denisa D.
- ORCID
- Venue
- Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 2016-12-28
- Volume
- 214
- Issue
- 2
- Pages
- 439-458
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- PMC
- PMC5294849
- OpenAlex
- W2562661149
- Cited by
- 218
- References
- 91
- Citations by year
- 2026: 14 · 2025: 23 · 2024: 36 · 2023: 28 · 2022: 20 · 2021: 25 · 2020: 22 · 2019: 21 · 2018: 19 · 2017: 10
- FWCI
- 10.11
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- The Journal of Experimental Medicine (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- GRO (submittedVersion)
- Funders
- National Heart, Lung, and Blood Institute (R01HL102101, R01HL125501, 5T32HL066987-13)
- Boston Children’s Hospital
- Deutsche Forschungsgemeinschaft (CH 1734/1-1)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Keywords
- PAD4, neutrophil extracellular traps, NETosis, myocardial fibrosis, pulmonary fibrosis, aging, inflammation, DNase1, platelet recruitment, pressure overload, collagen deposition, cardiac function
- MeSH terms
- Protein-Arginine Deiminase Type 4, Age Factors, Animals, Collagen, Fibrosis, Hydrolases, Mice, Inbred C57BL, Myocardium, Pulmonary Fibrosis, Ventricular Function, Left, Reactive Oxygen Species, Mice, Extracellular Traps
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