The DOI matches its Crossref record; 88 of the 88 references it cites were found in a registry or an index.
The Inflammation–Fibrosis Link? A Jekyll and Hyde Role for Blood Cells during Wound Repair
Open accessAbstract
The healing of a skin wound is a complex process involving many cell lineages. In adult tissues, repair is always accompanied by a robust inflammatory response, which is necessary to counter the potential for infection at any site where the skin barrier is breached. Unlike embryonic tissues that can repair perfectly without a remnant scar at the wound site, adult tissue repair always leads to formation of a fibrotic scar where the wound has healed. In recent years, it has become clear that the wound inflammatory response may be, at least in part, responsible for fibrosis at sites of tissue repair. In this review, we consider the beneficial vs the detrimental functions of inflammatory cells during the repair response and compare data from other tissues, the lung, and liver, where fibrosis and its resolution may be related to a damage-triggered inflammatory response. We also consider how it may be possible to molecularly disentangle the potentially good from the bad influences of inflammatory cells during tissue repair and how fundamental studies in inflammatory cell biology may prove the way forward for development of drug targets in this respect.
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“However, if ECM synthesis in myofibroblasts is not kept in check, then excessive matrix deposition can lead to fibrosis, scarring, and loss of tissue function [120–122].”
From CCN1/CYR61: the very model of a modern matricellular protein (2011) · cites this paper as [121]
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“At any rate, some studies could show that this reaction to a wound leads to an inferior defect closure, so the role of an immune response can be seen to be ambivalent.(57,61,62) As mentioned before, scar formation definitely does not replace intact skin in functional or aesthetic aspects.”
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The Multicomponent Medication Lymphomyosot Improves the Outcome of Experimental Lymphedema
Keim, A., Slis, J. R., Mendez, U., Stroup, E. M., Burmeister, Y., Tsolaki, N., Gailing, O., & Goldman, J. (2013) · Lymphatic Research and Biology · doi:10.1089/lrb.2012.0024 · Cited by 17
“Wound repair is a complex and well-orchestrated biological process consisting of three sequential phases, inflammation, proliferation/granulation, and remodeling.(15,20) It is the inflammatory phase with its vast array of growth factors and mediators produced by the influx of granulocytes and macrophages, that if not…”
InfluentialBlood Gene Expression Profiling of Breast Cancer Survivors Experiencing Fibrosis
Landmark‐Høyvik, H., Dumeaux, V., Reinertsen, K. V., Edvardsen, H., Fosså, S. D., & Børresen‐Dale, A. (2010) · International Journal of Radiation Oncology*Biology*Physics · doi:10.1016/j.ijrobp.2010.09.052 · Cited by 15
Nhu, Q. M., Hsieh, L. Y., Dohil, L., Dohil, R., Newbury, R., Kurten, R. C., Moawad, F. J., & Aceves, S. S. (2020) · Clinical and Translational Gastroenterology · doi:10.14309/ctg.0000000000000164 · Cited by 15
“Although inflammation is considered as the trigger for fibrosis, the inflammation-fibrosis connection may become uncoupled (42).”
BackgroundPotential Application of Non-flavonoid Phenolics in Diabetes: Antiinflammatory Effects
Miranda, J., Lasa, A., Aguirre, L., Fernández‐Quintela, A., Milton‐Laskibar, I., & Portillo, M. P. (2014) · Current Medicinal Chemistry · doi:10.2174/0929867321666140815123507 · Cited by 15
Regeneration-Competent and -Incompetent Murids Differ in Neutrophil Quantity and Function
Cyr, J. L., Gawriluk, T. R., Kimani, J. M., Rada, B., Watford, W. T., Kiama, S. G., Seifert, A. W., & Ezenwa, V. O. (2019) · Integrative and Comparative Biology · doi:10.1093/icb/icz023 · Cited by 14
Cyclooxygenase‐2 signaling in vocal fold fibroblasts
Branski, R. C., Zhou, H., Sandulache, V. C., Chen, J., Felsen, D., & Kraus, D. H. (2010) · The Laryngoscope · doi:10.1002/lary.21017 · Cited by 13
“suggests that the inflammatory response decreases with advancing age accompanied by reduced scarring.(17) These phenomena have been confirmed in various animal models.”
BackgroundDiabetic nephropathy: Treatment with phosphodiesterase type 5 inhibitors
Thompson, C. S. (2013) · World Journal of Diabetes · doi:10.4239/wjd.v4.i4.124 · Cited by 12
Walas, D., Nowicki-Osuch, K., Alibhai, D., Roloff, E. V. L., Coghill, J. A., Waterfall, C. M., & Paton, J. F. R. (2018) · Journal of Cerebral Blood Flow & Metabolism · doi:10.1177/0271678x18769180 · Cited by 12
“Residing macrophages and circulating monocytes may be the source of TGFb molecules with the ROS promoting the excessive scarring profile.(56,57) The inhibition of interferon signalling we found may be causal to, or agonise an existing, immune response.”
BackgroundRegulating Lymphatic Vasculature in Fibrosis: Understanding the Biology to Improve the Modeling
Ruliffson, B. N. K., & Whittington, C. F. (2023) · Advanced Biology · doi:10.1002/adbi.202200158 · Cited by 10
Targeting the myofibroblast to improve wound healing
Hinz, B. (2016) · Elsevier eBooks · doi:10.1016/b978-1-78242-455-0.00003-3 · Cited by 12
Zhang, Z., Wang, A., Wang, Y., Sun, W., Zhou, X., Xu, Q., Mao, L., & Zhang, J. (2023) · Molecules · doi:10.3390/molecules28083381 · Cited by 10
“The inflammatory response is tightly regulated in a highly coordinated network consisting of many cell types from both the innate and adaptive immune system, which mediate local responses to tissue damage and infections [18].”
BackgroundCurrent Concepts in Limb Regeneration
Wicker, J. F., & Kamler, K. (2009) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.2009.04413.x · Cited by 10
α7-nAChR Activation Has an Opposite Effect on Healing of Covered and Uncovered Wounds
Li, J.-Y., Jiang, S., Wang, L., Zhang, M.-Z., Wang, S., Jiang, Z., Liu, Y., Cheng, H., Zhang, M., Zhao, R., et al. (2017) · Inflammation · doi:10.1007/s10753-017-0703-5 · Cited by 10
“Inflammation is a double-edged sword; although excessive inflammation might inhibit tissue repair, adequate inflammation is critical for successful wound healing [41, 42, 49].”
BackgroundTissue regeneration in dentistry: Can salamanders provide insight?
Sader, F., Denis, J. P., & Roy, S. (2017) · Oral Diseases · doi:10.1111/odi.12674 · Cited by 9
Rapacz‐Leonard, A., Leonard, M., Chmielewska‐Krzesińska, M., Siemieniuch, M., & Janowski, T. E. (2020) · Scientific Reports · doi:10.1038/s41598-020-59085-1 · Cited by 9
Upregulation of Nrf2 in myocardial infarction and ischemia-reperfusion injury of the heart
Zuberi, S., Rafi, H., Hussain, A., & Hashmi, S. (2024) · PLoS ONE · doi:10.1371/journal.pone.0299503 · Cited by 8
“…myofibroblasts are active 4–7 days after ischemic injury and macrophages are also maximally activated seven days following ischemic insult, this makes one week time point ideal to study macrophage-fibroblast transition to cardiac fibrosis and the complications that result from it [32, 34].”
BackgroundEffect of Blood on Synovial Joint Tissues: Potential Role of Ferroptosis
Nicholson, H. J., Sakhrani, N., Rogot, J., Lee, A. J., Ojediran, I. G., Sharma, R., Chahine, N. O., Ateshian, G. A., Shah, R. P., & Hung, C. T. (2024) · Applied Sciences · doi:10.3390/app14146292 · Cited by 8
“Within a short time span, various immune cells are drawn from the blood that can release factors that influence neighboring cell behavior [64].”
Jagetia, G. C. (2017) · International Journal of Complementary & Alternative Medicine · doi:10.15406/ijcam.2017.09.00293 · Cited by 8
“The main aim of the injured tissue is to heal the wound as early as possible to avoid other detrimental consequences as a result the new tissue is not the exact replica of the original uninjured tissue [29].”
BackgroundJR5558 mice are a reliable model to investigate subretinal fibrosis
Seyed‐Razavi, Y., Lee, S., Fan, J., Shen, W., Cornish, E. E., & Gillies, M. C. (2024) · Scientific Reports · doi:10.1038/s41598-024-66068-z · Cited by 7
Effect of Long-term Hyperimmunization on the Presence of Mast Cells in the Endometrium of the Mare
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Inflammatory bowel disease and extracellular matrix: when victim becomes double agent
Sferra, R., Vetuschi, A., Latella, G., Cappariello, A., & Pompili, S. (2026) · Inflammation Research · doi:10.1007/s00011-026-02195-9 · Cited by 5
Role of matrix metalloproteases in pulmonary fibrosis
Pardo, A., & Selman, M. (2008) · Birkhäuser Basel eBooks · doi:10.1007/978-3-7643-8585-9_3 · Cited by 4
The potential therapeutic role of melatonin in organ fibrosis: a comprehensive review
Huang, W., Zheng, J., Wang, M., Du, L., Bai, L., & Tang, H. (2024) · Frontiers in Medicine · doi:10.3389/fmed.2024.1502368 · Cited by 7
“…and myofibroblasts produce aberrant matrix metalloproteinases (MMPs), disrupting the basement membrane of local tissues and releasing various cytokines and chemokines, thereby recruiting and activating more immune cells, including neutrophils, macrophages, T lymphocytes, and B lymphocytes (3, 20).”
Donaldson, K., & Poland, C. A. (2012) · Elsevier eBooks · doi:10.1016/b978-0-12-386940-1.00007-6 · Cited by 4
Franchini, A. (2016) · Elsevier eBooks · doi:10.1016/b978-0-12-803252-7.00020-5 · Cited by 4
Franco-Valencia, K., Nóbrega, I. B. C., Cantaruti, T., Barra, A., Klein, A., Azevedo-Jr, G. M., Costa, R. A., & Carvalho, C. R. (2022) · Brazilian Journal of Medical and Biological Research · doi:10.1590/1414-431x2021e11735 · Cited by 4
“The sequential progression of cellular and molecular interactions that occurs during wound healing in healthy conditions is predictable and begins with the activation of the blood coagulation cascade (hemostasis), leukocyte recruitment (inflammatory phase), keratinocyte proliferation, angiogenesis, and fibroblast acti…”
BackgroundCholet, J. (2022) · Current Research in Complementary & Alternative Medicine · doi:10.29011/2577-2201.100052 · Cited by 4
“Macrophages are also involved in the capacity of fibroblasts and keratinocytes to produce matrix proteinases and collagens [1-3].”
Deb, S., & Borah, A. (2024) · PharmaNutrition · doi:10.1016/j.phanu.2024.100419 · Cited by 3
Palacín-García, R., Goñi, L., & Río, T. G.-D. (2025) · Biomimetics · doi:10.3390/biomimetics10080491 · Cited by 3
“Certain bioactive materials can improve wound healing by reducing inflammation and promoting the growth of fibroblasts, keratinocytes, and other cells involved in skin repair [11,12].”
Metadata
- Authors
- Stramer, B. M., Mori, R., & Martin, P.
- Affiliations
- University of Bristol (GB)
- Corresponding author
- Stramer, Brian M.
- Venue
- Journal of Investigative Dermatology
- Publisher
- Elsevier BV
- Published
- 2007-05
- Volume
- 127
- Issue
- 5
- Pages
- 1009-1017
- ISSN
- 0022-202X (ISSN-L)
- OpenAlex
- W1996789266
- Cited by
- 251
- References
- 88
- Citations by year
- 2026: 7 · 2025: 7 · 2024: 15 · 2023: 11 · 2022: 7 · 2021: 5 · 2020: 8 · 2019: 8 · 2018: 22 · 2017: 12 · 2016: 19 · 2015: 11 · 2014: 16 · 2013: 16 · 2012: 13
- FWCI
- 2.24
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Journal of Investigative Dermatology (publishedVersion)
- PubMed (publishedVersion)
- Bristol Research (University of Bristol) (publishedVersion)
- Topics
- Health Sciences › Medicine › Surgery › Wound Healing and Treatments
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Keywords
- wound healing, skin fibrosis, inflammation, inflammatory cells, scar formation, tissue repair, pulmonary fibrosis, liver fibrosis, fibrosis resolution, therapeutic target
- MeSH terms
- Animals, Blood Cells, Cicatrix, Fibrosis, Humans, Inflammation, Liver Cirrhosis, Pulmonary Fibrosis, Skin, Wound Healing
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