Effect of glycaemic control on apoptosis in diabetic wounds

Rai, Neha; Suryabhan,; Ansari, Mohd Nazam; Kumar, Mukesh; Shukla, Vijay K.; Tripathi, Kamlakar

doi:10.12968/jowc.2005.14.6.26792

Cited by 50 publications

(32 citation statements)

References 4 publications

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“…Popularly, apoptosis index (AI) has been used to describe the density of apoptotic cells. [27][28][29] In this study, AI was defined as a percentage of the number of TUNELpositive tenocytes divided by the total number of tenocytes. The epitenon and endotenon areas were observed separately.…”

Section: Immunofluorescencementioning

confidence: 99%

Molecular Events of Cellular Apoptosis and Proliferation in the Early Tendon Healing Period

Chen

Cao

et al. 2010

The Journal of Hand Surgery

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Section: Immunofluorescencementioning

confidence: 99%

Molecular Events of Cellular Apoptosis and Proliferation in the Early Tendon Healing Period

Chen

Cao

et al. 2010

The Journal of Hand Surgery

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“…As depicted for fibroblasts, high glucose exerts a toxic effect on endothelial cells (Berlanga-Acosta et al, 2013). High glucose concentrations has been shown to disturb endothelial cell cycle, increase DNA damage, and delay endothelial cells replication, as inducing excessive cell death (Busik, Mohr, & Grant, 2008;Callaghan, Ceradini, & Gurtner, 2005;Hink et al, 2001;Rai et al, 2005). In this aspect, further research is required to establish the role of uPA and uPAr in the impaired wound healing among patients with hyperglycemia.…”

Section: Discussionmentioning

confidence: 99%

Hyperglycemia is associated with lower levels of urokinase-type plasminogen activator and urokinase-type plasminogen activator receptor in wound fluid

Akıncı

Terzi

Sevindik

et al. 2014

Journal of Diabetes and its Complications

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“…High glucose ambient has been shown to disturb endothelial cells cycle, disrupt tube formation, increase DNA damage, delay endothelial cells replication, and induce apoptosis [94]. In vitro models simulating "normoglycemia" and "hyperglycemia" have demonstrated that under a high glucose ambient, proliferation of dermal microvascular endothelial cells appear impaired [95] while apoptosis is enhanced [96] which may be related to the concomitant up-regulation of proinflammatory cytokines as TNF-α, death receptors TNF-R1 and Fas ligand in a variety of cultured endothelial cells [97].…”

Section: Diabetic Wound Endothelial Cellsmentioning

confidence: 99%

Type 2 Diabetes Mellitus (T2DM): Biological Overview from Pathways to Organelles and its Translation toward a Torpid Wound Healing Process

Guillen-Nieto¹,

Herrera-Martínez²

2013

J Diabetes Metab

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T2DM is a heterogeneous group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action, or both. Hyperglycemia may simply represent the tip of a broad series of molecular events from mitochondrial damages, to epigenetic and metabolic pathways deregulations. At the same time, hyperglycemia appears as the most proximal trigger for the onset and perpetual progression of multi-organ complications even under normoglycemic conditions. Thus, the initial hyperglycemic hit translates into a permanently harmful cellular imprinting as has been demonstrated in diabetic donors' cells after several passages and cultured in ideal conditions. The wound healing failure along with the inability of the innate immunity to control peripheral infections is the hybrid that determines that 85% of all non-traumatic lower extremity amputations are practiced in diabetic subjects. Diabetic wounds exhibit a complex networking of inflammatory cytokines, local proteases, cytotoxic reactive oxygen and nitrogen species and a polymicrobial biofilm that impose a stagnant phenotype. All these ingredients negatively impact on fibroblasts, endothelial cells and keratinocytes while paradoxically perpetuate the immuno-inflammatory infiltrate. Although the molecular fundamentals toward chronification have not been elucidated, it seems that different gene simultaneously converge to impose the wound cells a pro-senescent, pro-catabolic and pro-apoptotic phenotype given the lack of a "physiological tuning" of tyrosine kinase-dependent receptors due to their limited activation by insulin and local growth factors. Although recombinant growth factors and smart devices have been introduced during the last years the figures of amputations are still discouraging. Faults have been committed while selecting the appropriate growth factor and because of the "chronic" instinct to treat the chronic wounds topically, where bioavailability of the active principle is compromised by wound and bacterial biofilm proteases. The periodic intralesional infiltration of epidermal growth factor has proved to overcome this hurdle. Granulation tissue growth stimulation and wound healing capacity has been restored in diabetic patients by this procedure in several clinical trials and common clinical practice studies.

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Effect of glycaemic control on apoptosis in diabetic wounds

Cited by 50 publications

References 4 publications

Molecular Events of Cellular Apoptosis and Proliferation in the Early Tendon Healing Period

Molecular Events of Cellular Apoptosis and Proliferation in the Early Tendon Healing Period

Hyperglycemia is associated with lower levels of urokinase-type plasminogen activator and urokinase-type plasminogen activator receptor in wound fluid

Type 2 Diabetes Mellitus (T2DM): Biological Overview from Pathways to Organelles and its Translation toward a Torpid Wound Healing Process

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