Cellular senescence is a promising target for chronic wounds: a comprehensive review
- Burns & Trauma Vol. 8, Issue 1, (2020)
- 作者机构：
Institute of Rocket Force Medicine
- 作者简介：
- 基金信息：
DOI：10.1093/burnst/tkaa021
CLC：Published：2020，
Published Online：23 June 2020，
扫 描 看 全 文
Ziwen Wang, Chunmeng Shi, Cellular senescence is a promising target for chronic wounds: a comprehensive review, Burns & Trauma, Volume 8, 2020, tkaa021, https://doi.org/10.1093/burnst/tkaa021
摘要
Abstract
Chronic wounds include
but are not limited to
radiation ulcers
pressure ulcers
vascular ulcers and diabetic foot ulcers. These chronic wounds can persist for years without healing and severe ulcers may lead to amputation. Unfortunately
the underlying pathologies of refractory chronic wounds are not fully characterized
and new treatments are urgently needed. Recently
increasing evidence has indicated that cell senescence plays an important role in the development of chronic wounds
and preventing cell senescence or removing senescent cells holds promise as a new therapeutic strategy. In this review
we aim to probe these latest findings to promote the understanding of cellular senescence in the pathological process and potential management of chronic wounds.
关键词
Keywords
Chronic woundsCell senescenceTherapeutic agentSkin Mucosa
references
1.Brownrigg JR, Apelqvist J, Bakker K, Schaper NC, Hinchliffe RJ. Evidence-based management of PAD & the diabetic foot. Eur J Vasc Endovasc Surg. 2013;45:673–81.
2.Richmond NA, Maderal AD, Vivas AC. Evidence-based management of common chronic lower extremity ulcers. Dermatol Ther. 2013;26:187–96.
3.Frykberg RG, Banks J. Challenges in the treatment of chronic wounds. Adv Wound Care (New Rochelle). 2015;4:560–82.
4.Rice JB, Desai U, Cummings AK, Birnbaum HG, Skornicki M, Parsons NB. Burden of diabetic foot ulcers for medicare and private insurers. Diabetes Care. 2014;37:651–8.
5.Gurtner GC, Chapman MA. Regenerative medicine: charting a new course in wound healing. Adv Wound Care (New Rochelle). 2016;5:314–28.
6.Han G, Ceilley R. Chronic wound healing: a review of current management and treatments. Adv Ther. 2017;34:599–610.
7.Jones RE, Foster DS, Longaker MT. Management of Chronic Wounds-2018. JAMA. 2018;320:1481–2.
8.Mulder GD, Vande Berg JS. Cellular senescence and matrix metalloproteinase activity in chronic wounds. Relevance to debridement and new technologies. J Am Podiatr Med Assoc. 2002;92:34–7.
9.Telgenhoff D, Shroot B. Cellular senescence mechanisms in chronic wound healing. Cell Death Differ. 2005;12:695–8.
10.Stanley A, Osler T. Senescence and the healing rates of venous ulcers. J Vasc Surg. 2001;33:1206–11.
11.Wang Z, Chen Z, Jiang Z, Luo P, Liu L, Huang Y, et al. Cordycepin prevents radiation ulcer by inhibiting cell senescence via NRF2 and AMPK in rodents. Nat Commun. 2019;10:2538.
12.Wang H, Wang Z, Huang Y, Zhou Y, Sheng X, Jiang Q, et al. Senolytics (DQ) mitigates radiation ulcers by removing senescent cells. Front Oncol. 2020;9:1576. doi: 10.3389/fonc.2019.01576.
13.Rodrigues M, Kosaric N, Bonham CA, Gurtner GC. Wound healing: a cellular perspective. Physiol Rev. 2019;99:665–706.
14.Dekoninck S, Blanpain C. Stem cell dynamics, migration and plasticity during wound healing. Nat Cell Biol. 2019;21:18–24.
15.Darwin E, Tomic-Canic M. Healing chronic wounds: current challenges and potential solutions. Curr Dermatol Rep. 2018;7:296–302.
16.Eming SA, Martin P, Tomic-Canic M. Wound repair and regeneration: mechanisms, signaling, and translation. Sci Transl Med. 2014. doi: 10.1126/scitranslmed.3009337.
17.Sun BK, Siprashvili Z, Khavari PA. Advances in skin grafting and treatment of cutaneous wounds. Science. 2014;346:941–5.
18.Freedberg IM, Tomic-Canic M, Komine M, Blumenberg M. Keratins and the keratinocyte activation cycle. J Invest Dermatol. 2001;116:633–40.
19.Munoz-Espin D, Serrano M. Cellular senescence: from physiology to pathology. Nat Rev Mol Cell Biol. 2014;15:482–96.
20.Stadelmann WK, Digenis AG, Tobin GR. Physiology and healing dynamics of chronic cutaneous wounds. Am J Surg. 1998;176:26S–38.
21.Armstrong DG, Wrobel J, Robbins JM. Guest editorial: are diabetes-related wounds and amputations worse than cancer? Int Wound J. 2007;4:286–7.
22.Moffatt CJ, Franks PJ, Doherty DC, Smithdale R, Steptoe A. Psychological factors in leg ulceration: a case-control study. Br J Dermatol. 2009;161:750–6.
23.McCarty SM, Percival SL. Proteases and delayed wound healing. Adv Wound Care (New Rochelle). 2013;2:438–47.
24.Pastar I, Wong LL, Egger AN, Tomic-Canic M. Descriptive vs mechanistic scientific approach to study wound healing and its inhibition: is there a value of translational research involving human subjects? Exp Dermatol. 2018;27:551–62.
25.He S, Sharpless NE. Senescence in health and disease. Cell. 2017;169:1000–11.
26.Childs BG, Baker DJ, Kirkland JL, Campisi J, van Deursen JM. Senescence and apoptosis: dueling or complementary cell fates? EMBO Rep. 2014;15:1139–53.
27.Dunnill C, Patton T, Brennan J, Barrett J, Dryden M, Cooke J, et al. Reactive oxygen species (ROS) and wound healing: the functional role of ROS and emerging ROS-modulating technologies for augmentation of the healing process. Int Wound J. 2017;14:89–96.
28.Sousa-Victor P, Gutarra S, Garcia-Prat L, Rodriguez-Ubreva J, Ortet L, Ruiz-Bonilla V, et al. Geriatric muscle stem cells switch reversible quiescence into senescence. Nature. 2014;506:316–21.
29.Ogrodnik M, Salmonowicz H, Jurk D, Passos JF. Expansion and cell-cycle arrest: common denominators of cellular senescence. Trends Biochem Sci. 2019;44: 996–1008.
30.Li J, Song S, Li X, Zhu J, Li W, Du B, et al. Down-regulation of fibroblast growth factor 2 (FGF2) contributes to the premature senescence of mouse embryonic fibroblast. Med Sci Monit. 2020;26:e920520. doi: 10.12659/MSM.920520.
31.Satyanarayana A, Greenberg RA, Schaetzlein S, Buer J, Masutomi K, Hahn WC, et al. Mitogen stimulation cooperates with telomere shortening to activate DNA damage responses and senescence signaling. Mol Cell Biol. 2004;24:5459–74.
32.Wiley CD, Campisi J. From ancient pathways to aging cells-connecting metabolism and cellular senescence. Cell Metab. 2016;23:1013–21.
33.Campisi J. Aging, cellular senescence, and cancer. Annu Rev Physiol. 2013;75:685–705.
34.Coppe JP, Desprez PY, Krtolica A, Campisi J. The senescence-associated secretory phenotype: the dark side of tumor suppression. Annu Rev Pathol. 2010;5:99–118.
35.Sagiv A, Krizhanovsky V. Immunosurveillance of senescent cells: the bright side of the senescence program. Biogerontology. 2013;14:617–28.
36.Xue W, Zender L, Miething C, Dickins RA, Hernando E, Krizhanovsky V, et al. Senescence and tumour clearance is triggered by p53 restoration in murine liver carcinomas. Nature. 2007;445:656–60.
37.Hoenicke L, Zender L. Immune surveillance of senescent cells—biological significance in cancer- and non-cancer pathologies. Carcinogenesis. 2012;33:1123–6.
38.Acosta JC, Banito A, Wuestefeld T, Georgilis A, Janich P, Morton JP, et al. A complex secretory program orchestrated by the inflammasome controls paracrine senescence. Nat Cell Biol. 2013;15:978–90.
39.Hubackova S, Krejcikova K, Bartek J, Hodny Z. IL1- and TGFbeta-Nox4 signaling, oxidative stress and DNA damage response are shared features of replicative, oncogene-induced, and drug-induced paracrine ‘bystander senescence’. Aging. 2012;4:932–51.
40.Nelson G, Wordsworth J, Wang C, Jurk D, Lawless C, Martin-Ruiz C, et al. A senescent cell bystander effect: senescence-induced senescence. Aging Cell. 2012;11:345–9.
41.Kang C, Xu Q, Martin TD, Li MZ, Demaria M, Aron L, et al. The DNA damage response induces inflammation and senescence by inhibiting autophagy of GATA4. Science. 2015;349:aa5612.
42.Kuilman T, Michaloglou C, Vredeveld LC, Douma S, van Doorn R, Desmet CJ, et al. Oncogene-induced senescence relayed by an interleukin-dependent inflammatory network. Cell. 2008;133:1019–31.
43.Acosta JC, O’Loghlen A, Banito A, Guijarro MV, Augert A, Raguz S, et al. Chemokine signaling via the CXCR2 receptor reinforces senescence. Cell. 2008;133:1006–18.
44.Munoz-Espin D, Canamero M, Maraver A, Gomez-Lopez G, Contreras J, Murillo-Cuesta S, et al. Programmed cell senescence during mammalian embryonic development. Cell. 2013;155:1104–18.
45.Nacher V, Carretero A, Navarro M, Armengol C, Llombart C, Rodriguez A, et al. The quail mesonephros: a new model for renal senescence? J Vasc Res. 2006;43:581–6.
46.Storer M, Mas A, Robert-Moreno A, Pecoraro M, Ortells MC, Di Giacomo V, et al. Senescence is a developmental mechanism that contributes to embryonic growth and patterning. Cell. 2013;155:1119–30.
47.Besancenot R, Chaligne R, Tonetti C, Pasquier F, Marty C, Lecluse Y, et al. A senescence-like cell-cycle arrest occurs during megakaryocytic maturation: implications for physiological and pathological megakaryocytic proliferation. PLoS Biol. 2010;8. doi: 10.1371/journal.pbio.1000476.
48.Chuprin A, Gal H, Biron-Shental T, Biran A, Amiel A, Rozenblatt S, et al. Cell fusion induced by ERVWE1 or measles virus causes cellular senescence. Genes Dev. 2013;27:2356–66.
49.Kang TW, Yevsa T, Woller N, Hoenicke L, Wuestefeld T, Dauch D, et al. Senescence surveillance of pre-malignant hepatocytes limits liver cancer development. Nature. 2011;479:547–51.
50.Demaria M, Ohtani N, Youssef SA, Rodier F, Toussaint W, Mitchell JR, et al. An essential role for senescent cells in optimal wound healing through secretion of PDGF-AA. Dev Cell. 2014;31:722–33.
51.Yun MH, Davaapil H, Brockes JP. Recurrent turnover of senescent cells during regeneration of a complex structure. Elife. 2015;4:e05505:.
52.Huang T, Rivera-Perez JA. Senescence-associated beta-galactosidase activity marks the visceral endoderm of mouse embryos but is not indicative of senescence. Genesis. 2014;52:300–8.
53.Kim KH, Won JH, Cheng N, Lau LF. The matricellular protein CCN1 in tissue injury repair. J Cell Commun Signal. 2018;12:273–9.
54.Rinkevich Y, Walmsley GG, Hu MS, Maan ZN, Newman AM, Drukker M, et al. Skin fibrosis. Identification and isolation of a dermal lineage with intrinsic fibrogenic potential. Science. 2015;348:aaa2151.
55.Coppe JP, Patil CK, Rodier F, Sun Y, Munoz DP, Goldstein J, et al. Senescence-associated secretory phenotypes reveal cell-nonautonomous functions of oncogenic RAS and the p53 tumor suppressor. PLoS Biol. 2008;6:2853–68.
56.Schultz GS, Sibbald RG, Falanga V, Ayello EA, Dowsett C, Harding K, et al. Wound bed preparation: a systematic approach to wound management. Wound Repair Regen. 2003;11:S1–28.
57.Gordon S, Pluddemann A. Tissue macrophages: heterogeneity and functions. BMC Biol. 2017. doi: 10.1186/s12915-017-0392-4.
58.Rawji KS, Mishra MK, Michaels NJ, Rivest S, Stys PK, Yong VW. Immunosenescence of microglia and macrophages: impact on the ageing central nervous system. Brain. 2016;139:653–61.
59.von Kobbe C. Cellular senescence: a view throughout organismal life. Cell Mol Life Sci. 2018;75:3553–67.
60.Agren MS, Steenfos HH, Dabelsteen S, Hansen JB, Dabelsteen E. Proliferation and mitogenic response to PDGF-BB of fibroblasts isolated from chronic venous leg ulcers is ulcer-age dependent. J Invest Dermatol. 1999;112:463–9.
61.Bourguignon LY. Matrix hyaluronan-activated CD44 signaling promotes keratinocyte activities and improves abnormal epidermal functions. Am J Pathol. 2014;184:1912–9.
62.Cook H, Davies KJ, Harding KG, Thomas DW. Defective extracellular matrix reorganization by chronic wound fibroblasts is associated with alterations in TIMP-1, TIMP-2, and MMP-2 activity. J Invest Dermatol. 2000;115:225–33.
63.Wall IB, Moseley R, Baird DM, Kipling D, Giles P, Laffafian I, et al. Fibroblast dysfunction is a key factor in the non-healing of chronic venous leg ulcers. J Invest Dermatol. 2008;128:2526–40.
64.Vande Berg JS, Rose MA, Haywood-Reid PL, Rudolph R, Payne WG, Robson MC. Cultured pressure ulcer fibroblasts show replicative senescence with elevated production of plasmin, plasminogen activator inhibitor-1, and transforming growth factor-beta1. Wound Repair Regen. 2005;13:76–83.
65.Thomas CA, Holdstock JM, Harrison CC, Price BA, Whiteley MS. Healing rates following venous surgery for chronic venous leg ulcers in an independent specialist vein unit. Phlebology. 2013;28:132–9.
66.Bitar MS. The GSK-3beta/Fyn/Nrf2 pathway in fibroblasts and wounds of type 2 diabetes: on the road to an evidence-based therapy of non-healing wounds. Adipocyte. 2012;1:161–3.
67.Coalson E, Bishop E, Liu W, Feng Y, Spezia M, Liu B, et al. Stem cell therapy for chronic skin wounds in the era of personalized medicine: from bench to bedside. Genes Dis. 2019;6:342–58.
68.Maranda EL, Rodriguez-Menocal L, Badiavas EV. Role of Mesenchymal stem cells in dermal repair in burns and diabetic wounds. Curr Stem Cell Res Ther. 2017;12:61–70.
69.Ennis WJ, Sui A, Bartholomew A. Stem cells and healing: impact on inflammation. Adv Wound Care (New Rochelle). 2013;2:369–78.
70.Wang X, Chen Z, Luo S, Jin T, Wang Y, Chen F, et al. Development of therapeutic small-molecule Fluorophore for cell transplantation. Adv Funct Mater. 2016;26:8397–407.
71.Cianfarani F, Toietta G, Di Rocco G, Cesareo E, Zambruno G, Odorisio T. Diabetes impairs adipose tissue-derived stem cell function and efficiency in promoting wound healing. Wound Repair Regen. 2013;21:545–53.
72.Rodriguez-Menocal L, Salgado M, Ford D, Van Badiavas E. Stimulation of skin and wound fibroblast migration by mesenchymal stem cells derived from normal donors and chronic wound patients. Stem Cells Transl Med. 2012;1:221–9.
73.da Silva PFL, Ogrodnik M, Kucheryavenko O, Glibert J, Miwa S, Cameron K, et al. The bystander effect contributes to the accumulation of senescent cells in vivo. Aging Cell. 2019;18:e12848. doi: 10.1111/acel.12848.
74.Xu M, Pirtskhalava T, Farr JN, Weigand BM, Palmer AK, Weivoda MM, et al. Senolytics improve physical function and increase lifespan in old age. Nat Med. 2018;24:1246–56.
75.Ogrodnik M, Miwa S, Tchkonia T, Tiniakos D, Wilson CL, Lahat A, et al. Cellular senescence drives age-dependent hepatic steatosis. Nat Commun. 2017;8:15691.
76.Iglesias-Bartolome R, Patel V, Cotrim A, Leelahavanichkul K, Molinolo AA, Mitchell JB, et al. mTOR inhibition prevents epithelial stem cell senescence and protects from radiation-induced mucositis. Cell Stem Cell. 2012;11:401–14.
77.Le Roux I, Konge J, Le Cam L, Flamant P, Tajbakhsh S. Numb is required to prevent p53-dependent senescence following skeletal muscle injury. Nat Commun. 2015;6:8528.
0
Views
0
下载量
0
CSCD
- L-PDFDownload
- Meta-XMLDownload
- BibTeXDownload
- EndnoteDownload
- RefMan Download
- NoteExpressDownload
- NoteFirstDownload
Publicity Resources
Related Articles
Related Author
Related Institution
- Technical support is provided by Beijing Founder electronics co., LTD 京ICP备09064830号-19
京公网安备11010802024621 - It is recommended to read the content of this site in Chrome&IE9+. Please switch to extreme mode in browser 360.
- Cookies We use cookies to help provide and enhance our service and tailor content. By continuing, you agree to the use of cookies.
