The DOI matches its Crossref record; 15 of the 15 references it cites were found in a registry or an index.
Diabetic Wound-Healing Science
Open accessAbstract
Diabetes mellitus is an increasingly prevalent chronic metabolic disease characterized by prolonged hyperglycemia that leads to long-term health consequences. It is estimated that impaired healing of diabetic wounds affects approximately 25% of all patients with diabetes mellitus, often resulting in lower limb amputation, with subsequent high economic and psychosocial costs. The hyperglycemic environment promotes the formation of biofilms and makes diabetic wounds difficult to treat. In this review, we present updates regarding recent advances in our understanding of the pathophysiology of diabetic wounds focusing on impaired angiogenesis, neuropathy, sub-optimal chronic inflammatory response, barrier disruption, and subsequent polymicrobial infection, followed by current and future treatment strategies designed to tackle the various pathologies associated with diabetic wounds. Given the alarming increase in the prevalence of diabetes, and subsequently diabetic wounds, it is imperative that future treatment strategies target multiple causes of impaired healing in diabetic wounds.
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Cites
Factors affecting wound healing
Guo, S., & DiPietro, L. A. (2010) · Journal of Dental Research · doi:10.1177/0022034509359125 · Cited by 5,792
Sindrilaru, A., Peters, T., Wieschalka, S., Baican, C., Baican, A., Peter, H., Hainzl, A., Schatz, S., Qi, Y., Schlecht, A., et al. (2011) · Journal of Clinical Investigation · doi:10.1172/jci44490 · Cited by 1,100 · cited 1×
“…are characterized by the non-resolving inflammation phase, where a large number of neutrophils and macrophages are found in the wound bed [85,88,89], as well as the chronic release of proinflammatory cytokines including interleukin (IL)-1, IL-6, tumor necrosis factor (TNF)- α, and plasma C…”
BackgroundInteractions of cytokines, growth factors, and proteases in acute and chronic wounds
Mast, B. A., & Schultz, G. S. (1996) · Wound Repair and Regeneration · doi:10.1046/j.1524-475x.1996.40404.x · Cited by 598 · cited 1×
“Moreover, DFUs often exhibit deregulation and mislocalization of GF receptors [227–229], as well compartmentalization within microdomains (i.e., cave-olae), which prevent activation of downstream signaling events [230–232].”
BackgroundDermal adipocytes protect against invasive Staphylococcus aureus skin infection
Zhang, L.-J., Guerrero-Juarez, C. F., Hata, T., Bapat, S. P., Ramos, R., Plikus, M. V., & Gallo, R. L. (2015) · Science · doi:10.1126/science.1260972 · Cited by 471
Pastar, I., Nusbaum, A. G., Gil, J., Patel, S. B., Chen, J., Valdes, J., Stojadinovic, O., Plano, L. R., Tomic-Canic, M., & Davis, S. C. (2013) · PLoS ONE · doi:10.1371/journal.pone.0056846 · Cited by 391
The Innate Immune System in Acute and Chronic Wounds
MacLeod, A. S., & Mansbridge, J. N. (2016) · Advances in Wound Care · doi:10.1089/wound.2014.0608 · Cited by 289 · cited 3×
“The healing dynamics in acute wounds consist of four overlapping phases, including hemostasis, inflammation, proliferation, and remodeling [85,86].”
BackgroundEdmonds, M., Lázaro-Martínez, J. L., Alfayate-García, J. M., Martini, J., Petit, J.-M., Rayman, G., Lobmann, R., Uccioli, L., Sauvadet, A., Bohbot, S., et al. (2018) · The Lancet Diabetes & Endocrinology · doi:10.1016/s2213-8587(17)30438-2 · Cited by 275
Beidler, S. K., Douillet, C. D., Berndt, D. F., Keagy, B. A., Rich, P. B., & Marston, W. A. (2009) · Journal of Vascular Surgery · doi:10.1016/j.jvs.2008.11.049 · Cited by 223 · cited 1×
“tumor necrosis factor (TNF)-α, and plasma C reactive protein [85,88,90,91], and bacterial proliferation [88,92] being the most explored factors that contribute to the impaired healing process.”
BackgroundMacrophage PPARγ and impaired wound healing in type 2 diabetes
Mirza, R. E., Fang, M. M., Novak, M. L., Urao, N., Sui, A., Ennis, W. J., & Koh, T. J. (2015) · The Journal of Pathology · doi:10.1002/path.4548 · Cited by 177 · cited 1×
“Macrophages are widely investigated when studying the immune system in chronic wounds of diabetic humans and mice in part because they produce and release cytokines, are influenced by the surrounding microbiome, and coordinate the transition from the inflammatory to proliferative phase [108–111].”
BackgroundMicroRNA signature in diabetic wound healing: promotive role of miR‐21 in fibroblast migration
Madhyastha, R., Madhyastha, H., Nakajima, Y., Omura, S., & Maruyama, M. (2012) · International Wound Journal · doi:10.1111/j.1742-481x.2011.00890.x · Cited by 168
Cited by
Cai, Y., Chen, K., Liu, C., & Qu, X. (2023) · Bioactive Materials · doi:10.1016/j.bioactmat.2023.04.019 · Cited by 112
Extracellular matrix-inspired biomaterials for wound healing
Hosty, L., Heatherington, T., Quondamatteo, F., & Browne, S. (2024) · Molecular Biology Reports · doi:10.1007/s11033-024-09750-9 · Cited by 63
Wang, Z., Li, B., Nie, C., Zhang, R., Qu, S., Shao, Q., Zhang, X., Li, J., Li, W., Li, H., et al. (2025) · Nano Letters · doi:10.1021/acs.nanolett.4c06284 · Cited by 46
Li, Z., Dong, H., Yang, S., Wang, X., & Li, Z. (2025) · International Journal of Nanomedicine · doi:10.2147/ijn.s504924 · Cited by 12
“1,4 Conventional treatments, such as blood sugar control and surgical intervention, fail to accelerate wound healing, necessitating repeated treatments that impose financial and emotional strain on patients.”
Metadata
- Authors
- Burgess, J. L., Wyant, W. A., Abdo Abujamra, B., Kirsner, R. S., & Jozic, I.
- Venue
- Medicina
- Publisher
- MDPI AG
- Published
- 2021-10-08
- Volume
- 57
- Issue
- 10
- Pages
- 1072
- ISSN
- 1010-660X (ISSN-L)
- 1648-9144
- OpenAlex
- W3206629031
- Cited by
- 928
- References
- 15
- FWCI
- 42.11
- Type
- journal article
- Language
- en
- Open access
- gold
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- Burgess, J. L., Wyant, W. A., Abdo Abujamra, B., Kirsner, R. S., & Jozic, I. (2021). Diabetic Wound-Healing Science. Medicina. https://doi.org/10.3390/medicina57101072
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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