Diabetes per se is a complex disease. These experiments have suggested that high glucose concentration is the proximal detonator of a downstream cascade of molecular disturbances for the skin fibroblasts [14]. It is therefore evident that keratinocytes migration incapability plays an important role in re-epithelialization failure, since cytoskeletal keratins K2, K6 and K10 have been found diminished in DFUs []. Endothelial function and oxidative stress in cardiovascular diseases. Vascular endothelial growth factor-A-induced chemotaxis of monocytes is attenuated in patients with diabetes mellitus: High glucose-induced alterations of extracellular matrix of human skin fibroblasts are not dependent on TSPTGFbeta1 pathway. The global burden of diabetic foot disease.

As mentioned, these wounds are characterized by a proliferative arrest, pro-inflamed, pro-oxidant and pro-degradative phenotype [75]. Improved diabetic wound healing through topical silencing of p53 is associated with augmented vasculogenic mediators. J Cardiovasc Pharmacol 17, SS, Microparticles, Vascular Function and Atherothrombosis. This poor-healing condition appears to be a multifactorial process which includes the amalgamation of systemic and local factors that ensure a perpetual forward loop up to chronification. Log In Sign Up.

The pathogenic effects of hyperglycemia on fibroblasts and endothelial cells are summarized in figure 1.

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Fibronectin degradation, for instance, is referred as one among the several causes of diabetic re-epithelialization failure. Cellular dysfunction in the diabetic fibroblast: Liver sinusoidal endothelial cells: Magentic tagging of cell-derived microparticles: Interactions of cytokines, growth factors, and proteases in acute and chronic wounds.

In a broad systemic context, inflammation and anabolic deficit can be conceptually mentioned. A prospective study of the utility of plasma biomarkers to diagnose alcoholic hepatitis Hepatology66 2: Insulin and endothelial function: Finally, our basic research is complemented by translational activities in clinical studies in association with Paris Hospitals.


Vascular renin angiotensin system and endothelial function: We have included a characterization of the organizational disorders affecting diabetic granulation tissue and the challenge that represents its ultimate process, wound re-epithelialization.

Future Lipidology,2: Glucose has shown to exhibit a direct toxic effect on keratinocytes. Fadini GP, Avogaro A. The failure of wound contraction is a clinical hallmark of diabetic granulation tissue.

William Benessiano

This is associated to a decrease in cell directionality and to non-productive protrusive events e. Epub Aug These results indicated that p38 is a key signaling molecule that curiculum an opposite role during times of cellular growth and cellular stress vitaf. This is a family of transcription factors with apparently opposing roles that may defend cells against oxidative stress but also promote cell-cycle arrest in G1 by inducing the cell cycle inhibitory protein p27 kip1 [36].

Radiology, ; epub Feb13 ; 1: Influence of endothelial surface on flow velocity in vitro. Shear stress regulates endothelial microparticle release. The fact that these fibroblasts fail in secreting NO is particularly negative given its role for wound healing.

There is an enormous and ever-growing body of evidence indicating the close correlation between hyperglycemia and the abnormalities in endothelial function and cuericulum [41]. Mechanisms underlying endothelial dysfunction in diabetes mellitus.


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Chronic exposure of endothelial cells to eicosapentaenoic acid potentiates the release of endothelium-derived relaxing factor s. Gi proteins mediating the response to serotonin in cultured endothelial cells with impaired release of relaxing factors.

A case of perforating ulcers of both feet associated with diabetes and ataxic symptoms. Circulating microparticles and procoagulant activity in the elderly. Therefore, ROS appear to play a pivotal role in systemic endothelial deterioration and biological aging [62]. Systeme kinine kallikreine dans les maladies cardiovasculaires. Under this ambient, the expression of the proapoptotic Bax protein increases, cytochrome c is released, subsequently conjugating to the apoptotic protease activating factor-1 and triggering a caspase cascade-induced death [55].

Endothelial progenitor cell dysfunction: Curricuulum glucose concentrations have been associated with endothelial metabolic dysfunction in vitro and in vivo and as for multiple physiological processes; insulin and its downstream signaling regulate most of the endothelial cell functions [50].

william benessiano curriculum vitae

Fibrocytes contribute to the myofibroblast population in wounded skin and originate from the bone marrow.