The Nrf2/Keap1/ARE Pathway and Oxidative Stress as a Therapeutic Target in Type II Diabetes Mellitus.

Existing Reviews

Please note, new claims can take a short while to show up.

No claims yet.

Annotation Summary

Term Occurence Count Dictionary
hypoglycemia 1 endocrinologydiseases
obesity 4 endocrinologydiseases
Insulin 2 endocrinologydiseasesdrugs
diabetes mellitus 5 endocrinologydiseases
diabetic retinopathy 1 endocrinologydiseases
hyperglycemia 9 endocrinologydiseases

Graph of close proximity drug and disease terms (within 200 characters).

Note: If this graph is empty, then there are no terms that meet the proximity constraint.

Review

Having read the paper, please pick a pair of statements from the paper to indicate that a drug and disease are related.

Select Drug Character Offset Drug Term Instance
Insulin 15130 β-cells into these insulin-negative cell types under conditions of oxidative stress [[58]].5. Nrf2 and Insulin ResistanceIn addition to β-cell dysfunction, insulin resistance in a wide range of tissues is a hallmark
Insulin 40932 [[71], [79]]Heart failure(i) Aberrant cardiac and ECM remodeling(i) Blood pressure regulation [[72]](ii) Insulin resistance of myocytes(ii) Protection of myocardium following ischemia(iii) Impaired regulation of intracellular
Select Disease Character Offset Disease Term Instance
diabetes mellitus 478 /2017Publication date (epub): 8/2017AbstractDespite improvements in awareness and treatment of type II diabetes mellitus (TIIDM), this disease remains a major source of morbidity and mortality worldwide, and prevalence continues
diabetes mellitus 1487 target for prevention, prognosis, and treatment of TIID.1. IntroductionThe worldwide prevalence of diabetes mellitus (DM) was estimated at 8.5% in 2014, and the morbidity resulting from the microvascular and macrovascular
diabetes mellitus 1924 The chronic hyperglycemia and impairments in insulin secretion and action that characterize type II diabetes mellitus (TIIDM) are associated with long-term damage, dysfunction, and failure of many organs, including the
diabetes mellitus 20351 be associated with worsening coronary atherosclerosis in an autopsy study of Japanese patients with diabetes mellitus [[84]]. This seeming contradiction might be explained by a differential response of Nrf2 to laminar
diabetes mellitus 38910 therapeutic value in combatting this devastating disease.Figure 1The Nrf2/Keap1/ARE pathway in type II diabetes mellitus . (A) Under nonstressed conditions, the Nrf2 transcription factor is covalently bound to cysteine residues
diabetic retinopathy 42876 Keap1 cysteine residues/activation of upstream kinases(i) Prevented glucose-induced impairments in diabetic retinopathy [[142]]Cinnamic aldehyde (CA)Natural (found in bark of cinnamon tree)Activation of upstream kinases(i)
hyperglycemia 1836 alone, making it the most expensive medical condition by a significant margin [[2]–[4]]. The chronic hyperglycemia and impairments in insulin secretion and action that characterize type II diabetes mellitus (TIIDM)
hyperglycemia 10649 aforementioned pathways underlying the pathogenesis of diabetic complications has been tied to a singular hyperglycemia -induced event in the mitochondria, overproduction of superoxide by the electron-transport chain [[13]].
hyperglycemia 10891 have shown that the absence of Nrf2 may exacerbate both type I and type II diabetes [[33], [34]]. This hyperglycemia -specific increase in ROS overproduction by the mitochondria may explain why classic antioxidants, low
hyperglycemia 17643 [[66]]. Free radical-induced endothelial damage is thought to be the initiating step in CVD [[67]], and hyperglycemia -induced ROS in TIIDM exacerbates impairments in angiogenesis and neovascularization through means such
hyperglycemia 19675 located at atherosusceptible sites, conferring them a protective advantage in response to diabetic hyperglycemia [[71], [79]]. The significance of these effects is largely attributed to the downstream activation of
hyperglycemia 24408 unknown.6.4. Diabetic NephropathyDiabetic nephropathy is a well-known microvascular complication of chronic hyperglycemia , and both oxidative stress and an impaired response by the Nrf2/Keap1/ARE system have been implicated
hyperglycemia 24832 suppressed nephropathy and significantly improved metabolic indices associated with TIIDM, such as hyperglycemia , polydipsia, polyuria, and weight loss [[110]]. These benefits can be largely attributed to decreases
hyperglycemia 26832 mice [[118], [119]]. Interestingly, recent work in tissue regeneration models has demonstrated that hyperglycemia in diabetes is associated with Keap1 dysfunction, which prevents nuclear localization of Nrf2 and thus
hyperglycemia 44464 Protected against nephrotoxicity [[155]]∗HDL: high-density lipoprotein; ∗∗HbA1c: a marker of chronic hyperglycemia
hypoglycemia 15378 blood glucose levels and exacerbation of pancreatic damage as it attempts to compensate for perceived hypoglycemia . Studies by Uruno et al. in murine models of Nrf2 over-expression via both genetic Keap1 knockdown and
obesity 15619 suggest that Nrf2 activation can improve insulin sensitivity in diabetes and abrogate diabetes and obesity in mice [[44]]. Body weight and blood glucose levels were decreased in diabetic mice with Keap1 knockout.
obesity 16683 in the hypothalamus, a phenomenon that may affect systemic metabolic regulation [[59]]. Furthermore, obesity is associated with an increased risk of developing insulin resistance and TIIDM, and murine studies
obesity 31260 highly promising results in animal models of heart failure [[102]], insulin resistance [[52]], and obesity [[155]]. Bardoxolone methyl (CDDO-Me), one such derivative originally developed as an anticancer drug,
obesity 33409 of glucose and lipid metabolism, in mice [[159]]. This may have implications in guiding treatment of obesity in TIIDM, which is itself regulated, at least in part, by Nrf2 action on lipogenic gene expression and

You must be authorized to submit a review.