Diabetic neuropathy and oxidative stress: Therapeutic perspectives

Hosseini, A. and Abdollahi, M. (2013) Diabetic neuropathy and oxidative stress: Therapeutic perspectives. Oxidative Medicine and Cellular Longevity.

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Diabetic neuropathy (DN) is a widespread disabling disorder comprising peripheral nerves' damage. DN develops on a background of hyperglycemia and an entangled metabolic imbalance, mainly oxidative stress. The majority of related pathways like polyol, advanced glycation end products, poly-ADP-ribose polymerase, hexosamine, and protein kinase c all originated from initial oxidative stress. To date, no absolute cure for DN has been defined; although some drugs are conventionally used, much more can be found if all pathophysiological links with oxidative stress would be taken into account. In this paper, although current therapies for DN have been reviewed, we have mainly focused on the links between DN and oxidative stress and therapies on the horizon, such as inhibitors of protein kinase C, aldose reductase, and advanced glycation. With reference to oxidative stress and the related pathways, the following new drugs are under study such as taurine, acetyl-L-carnitine, alpha lipoic acid, protein kinase C inhibitor (ruboxistaurin), aldose reductase inhibitors (fidarestat, epalrestat, ranirestat), advanced glycation end product inhibitors (benfotiamine, aspirin, aminoguanidine), the hexosamine pathway inhibitor (benfotiamine), inhibitor of poly ADP-ribose polymerase (nicotinamide), and angiotensin-converting enzyme inhibitor (trandolapril). The development of modern drugs to treat DN is a real challenge and needs intensive long-term comparative trials. © 2013 Asieh Hosseini and Mohammad Abdollahi.

Item Type: Article
Additional Information: cited By 59
Uncontrolled Keywords: Advanced glycation end products; Aldose reductase inhibitors; Angiotensin-converting enzyme; Diabetic neuropathy; Pathophysiological; Pathway inhibitors; Peripheral nerves; Protein kinase C inhibitors, Amino acids; Enzymes; Glycosylation; Proteins, Oxidative stress, acetylcarnitine; acetylsalicylic acid; aminoguanidine; amitriptyline; benfotiamine; carbamazepine; citalopram; clomipramine; desipramine; duloxetine; epalrestat; fidarestat; fluphenazine; gabapentin; harkoseride; imipramine; lamotrigine; maprotiline; nicotinamide; nortriptyline; oxcarbazepine; pregabalin; ranirestat; ruboxistaurin; taurine; thioctic acid; trandolapril; unindexed drug; valproic acid; venlafaxine, bedtime dosage; blood glucose monitoring; clinical feature; diabetic neuropathy; drug dose titration; dyslipidemia; glucose blood level; glycemic control; human; hyperglycemia; inflammation; nerve fiber; neuropathic pain; nonhuman; oxidative stress; review; signal transduction; animal; pathology; pathophysiology, Animals; Diabetic Neuropathies; Humans; Oxidative Stress
Subjects: WK Endocrine System
Depositing User: somayeh pourmorteza
Date Deposited: 14 May 2019 09:45
Last Modified: 14 May 2019 09:45
URI: http://eprints.iums.ac.ir/id/eprint/9693

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