For instance, AGE can inhibit the growth of collagen, causing it become thickened, as well as endothelium, causing an induced growth inhibition and increased rate of apoptosis, especially in that of retinal cells. (M. Balasubramanyam,. Etel 2012) AGE complexes are very confirmative and stable at the physiological level in the human body where their rate of accumulation and dispersion in tissues, especially endothelial and adipose, depend on various components, including that of ions, modified proteins and chemical balances. (Alan W. Stitt 2010) Due to their maintainable stability in the physiological setting, AGEs are capable of causing severe consequences and damage, due to their ability to ...view middle of the document...
(David A. Antonetti Etel, 2006) The mechanisms to perform normal vision require intact cell-cell communication, involving the neuronal, microglial, glial vascular and epithelial cells, in correlation together where mechanism involving AGE and this disruption break this collection of components in a biosynthetic pathway. In addition, AGE, can further bind to immunoglobulin protein receptors, associated with AGE and produce a surge of signaling series, leading to a dysfunction in retinal cells due to the unique physiology and structure of the retina having precise, specialized build were its metabolic functions are compartmentalized, comprising between neurons and glia, much like the brain. (David A. Antonetti Etel, 2006)
Advanced glycation end products are critical through the mechanisms of AGE-mediated programmed cell death of meningeal cells, and altered extracellular matrix proteins, present in contribution to both glomerular hyper-filtration and sclerosis. The actual formation of AGE is also known to stimulate the over secretion of growth factors in those such as insulin-like growth factor 1 and transforming growth factor beta, which further contribute to glomerular fibrosis, with a result guiding implication of decreased availability in glomerular surface area for filtration. (David A. Antonetti Etel, 2006)
Diabetic nephropathy is the chronic condition secondary to hyperglycemia, and possibly influenced by hypertension, depending on the individual themselves, where the hyperglycemia induces dysfunction in cells associated and functioning in the kidneys, ultimately leading to stages of renal dysfunction to progression of renal failure. Both type 1 and 2 diabetes mellitus are obviously diverse in pathology and in the mechanisms in which the metabolic disorder proceeds, however, similarly, the physiological changes that result from diabetes impacts various tissues of the renal system, including the glomerulus, tubointerstitium and vasculature, comprising the majority of the system.
(Gunter Wolf, Fuad N. Ziyhadeh, 1999) Due to the etiology of the tissue in the kidneys arising from mesangial, endothelial and glomerular podocytes, along with interstitial fibroblasts, these cells are impacted due the susceptibility to hyperglycemia, implying that diabetes mellitus can affect these tissues to different degrees or extents, resulting in different stages of the renal dysfunction and subsequent failure. The cellular and molecular components involved in renal function and response have been demonstrated to show that the elements in these pathways respond to hyperglycemia in similar mechanisms via activating similar signaling pathways or occurrences with variations depending on if a molecule in a cell is present, absent and or expressed. (Yashpal S. Kanwar, Etel, 2013)
Molecules, including aldose reductase in PKC pathways produce intracellular events where such components become induced in the presence of high glucose levels where an...