Oxidative Stress and “Senescent” Fibroblasts in Non-Healing Wounds as Potential Therapeutic Targets

Clark, Richard A F
October 2008
Journal of Investigative Dermatology;Oct2008, Vol. 128 Issue 10, p2361
Academic Journal
In chronic wounds, fibroblast dysfunctions, such as increased apoptosis, premature senescence, senescence-like phenotype, or poor growth response in the absence of senescence markers, have been reported. Some of these differential dysfunctions may be secondary to differences in patient age or sex, ulcer size or duration, edge versus base sampling, or culture technique. Nevertheless, the entire spectrum of fibroblast dysfunction may exist and be secondary to, or a response to, different amounts of oxidative stress.Journal of Investigative Dermatology (2008) 128, 2361–2364. doi:10.1038/jid.2008.257


Related Articles

  • Protective effect of geraniol inhibits inflammatory response, oxidative stress and apoptosis in traumatic injury of the spinal cord through modulation of NF-κB and p38 MAPK. JIANSHENG WANG; BAISHAN SU; HONGBIN ZHU; CHAO CHEN; GANG ZHAO // Experimental & Therapeutic Medicine;Dec2016, Vol. 12 Issue 6, p3607 

    Geraniol is a type of monoterpenoid with a rose scent and a slightly sweet flavor. It is found in the volatile oil of various plants, and has anti-inflammatory and anti-oxidant effects. The present study aimed to investigate the protective effect of geraniol in inhibiting the inflammatory...

  • Diabetes Enhances mRNA Levels of Proapoptotic Genes and Caspase Activity, Which Contribute to Impaired Healing. Al-Mashat, Hesham A.; Kandru, Suneel; Liu, Rongkun; Behl, Yugal; Desta, Tesfahun; Graves, Dana T. // Diabetes;Feb2006, Vol. 55 Issue 2, p487 

    We previously reported that after a bacteria-induced wound in the scalp, type 2 diabetic (db/db) mice had higher levels of apoptosis of fibroblasts and bone-fining cells that are critical for healing compared with normoglycemic controls. To investigate mechanisms by which this might occur, RNA...

  • CHAPTER 4: The potential effect of fibroblast senescence on wound healing and the chronic wound environment. Henderson, E. A. // Trends in Wound Care - Volume 5;2008, Vol. 5, p47 

    Chapter 4 of the book "Trends in Wound Care" Volume V, edited by Keith F. Cutting is presented. It discusses the impact of fibroblast cell senescence on chronic wound healing. It highlights how wound environment contributes to the increment of oxidative stress and pro-inflammatory cytokines...

  • Impairment of Lon-Induced Protection Against the Accumulation of Oxidized Proteins in Senescent Wi-38 Fibroblasts. Ngo, Jenny K.; Pomatto, Laura C. D.; Bota, Daniela A.; Koop, Alison L.; Davies, Kelvin J. A. // Journals of Gerontology Series A: Biological Sciences & Medical ;Nov2011, Vol. 66A Issue 11, p1178 

    Oxidative damage to mitochondrial proteins is thought to contribute to the aging process, but the Lon protease normally degrades such proteins. In early-passage WI-38 human lung fibroblasts, Lon expression is rapidly induced during H2O2 stress, which prevents the accumulation of oxidized...

  • Aloin Protects Skin Fibroblasts from Heat Stress-Induced Oxidative Stress Damage by Regulating the Oxidative Defense System. Liu, Fu-Wei; Liu, Fu-Chao; Wang, Yu-Ren; Tsai, Hsin-I; Yu, Huang-Ping // PLoS ONE;12/4/2015, Vol. 10 Issue 12, p1 

    Oxidative stress is commonly involved in the pathogenesis of skin damage induced by environmental factors, such as heat stress. Skin fibroblasts are responsible for the connective tissue regeneration and the skin recovery from injury. Aloin, a bioactive compound in Aloe vera, has been reported...

  • Cellular senescence: unravelling complexity. Passos, João F.; Simillion, Cedric; Hallinan, Jennifer; Wipat, Anil; Von Zglinicki, Thomas // Age;Dec2009, Vol. 31 Issue 4, p353 

    Cellular senescence might be a tumour suppressing mechanism as well as a contributor to age-related loss of tissue function. It has been characterised classically as the result of the loss of DNA sequences called telomeres at the end of chromosomes. However, recent studies have revealed that...

  • The Autistic Phenotype Exhibits a Remarkably Localized Modification of Brain Protein by Products of Free Radical-Induced Lipid Oxidation. Evans, Teresa A.; Siedlak, Sandra L.; Liang Lu; Xiaoming Fu; Zeneng Wang; McGinnis, Woody R.; Fakhoury, Evelyn; Castellani, Rudy J.; Hazen, Stanley L.; Walsh, William J.; Lewis, Allen T.; Salomon, Robert G.; Smith, Mark A.; Perry, George; Xiongwei Zhu // American Journal of Biochemistry & Biotechnology;2008, Vol. 4 Issue 2, p61 

    Oxidative damage has been documented in the peripheral tissues of autism patients. In this study, we sought evidence of oxidative injury in autistic brain. Carboxyethyl pyrrole (CEP) and iso[4]levuglandin (iso[4]LG)E2-protein adducts, that are uniquely generated through peroxidation of...

  • Melatonin is able to delay endoplasmic reticulum stress-induced apoptosis in leukocytes from elderly humans. Espino, Javier; Bejarano, Ignacio; Paredes, Sergio; Barriga, Carmen; Reiter, Russel; Pariente, José; Rodríguez, Ana // Age;Dec2011, Vol. 33 Issue 4, p497 

    The mechanisms regulating neutrophil apoptosis are basically unaffected by the aging process. However, a significant impairment of cell survival occurs in elderly individuals following neutrophil challenge with pro-inflammatory stimuli, such as granulocyte-macrophage colony-stimulating factor...

  • Release of mitochondrial apoptogenic factors and cell death are mediated by CK2 and NADPH oxidase. Kim, Gab Seok; Jung, Joo Eun; Narasimhan, Purnima; Sakata, Hiroyuki; Yoshioka, Hideyuki; Song, Yun Seon; Okami, Nobuya; Chan, Pak H // Journal of Cerebral Blood Flow & Metabolism;Apr2012, Vol. 32 Issue 4, p720 

    Activation of the NADPH oxidase subunit, NOX2, and increased oxidative stress are associated with neuronal death after cerebral ischemia and reperfusion. Inhibition of NOX2 by casein kinase 2 (CK2) leads to neuronal survival, but the mechanism is unknown. In this study, we show that in...


Read the Article


Sorry, but this item is not currently available from your library.

Try another library?
Sign out of this library

Other Topics