Evidence map›Paper›PMID 22025779›Full record

ArticleDiabetes2011

Therapeutic potential of Nrf2 activators in streptozotocin-induced diabetic nephropathy.

Hongting Zheng, Samantha A Whitman, Wei Wu, Georg T Wondrak, Pak K Wong, Deyu Fang, Donna D Zhang

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 250 papers.

0numbers the graph read from it
0cells of the map it votes in
250citing papers in PubMed
11.3field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

250 citing papers in PubMed, 499 citations in OpenAlex.

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  20. Molecular Therapeutics for Diabetic Kidney Disease: An Update.International journal of molecular sciences · 2024
    Review

190 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 2 countries.

Hongting ZhengDepartment of Pharmacology and Toxicology, University of Arizona, Tucson, Arizona, USA.
Samantha A Whitman
Wei Wu
Georg T Wondrak
Pak K Wong
Deyu Fang
Donna D Zhang
University of Arizona · USArmy Medical University · CNNorthwestern University · USXinqiao Hospital · CN

Funding

SOUTHWEST ENVIRONMENTAL HEALTH SCIENCES CENTERP30ES006694 · NIEHS · UNIVERSITY OF ARIZONA · PI DEAN BILLHEIMER · 1994 to 2026
$36.7M
Training in Environmental Toxicology of Human DiseaseT32ES007091 · NIEHS · UNIVERSITY OF ARIZONA · PI Nathan J Cherrington · 1985 to 2026
$10.7M
The protective role of Nrf2 in arsenic-induced toxicity and carcinogenicityR01ES015010 · NIEHS · UNIVERSITY OF ARIZONA · PI ZHANG, DONNA D · 2006 to 2015
$3.4M
NIEHS NIH HHS ES015010NIEHS NIH HHS P30 ES006694NIEHS NIH HHS R01 ES015010NIEHS NIH HHS T32 ES007091
6 · The paper itself

Abstract

objectiveTo determine whether dietary compounds targeting NFE2-related factor 2 (Nrf2) activation can be used to attenuate renal damage and preserve renal function during the course of streptozotocin (STZ)-induced diabetic nephropathy. RESEARCH DESIGN AND

methodsDiabetes was induced in Nrf2(+/+) and Nrf2(-/-) mice by STZ injection. Sulforaphane (SF) or cinnamic aldehyde (CA) was administered 2 weeks after STZ injection and metabolic indices and renal structure and function were assessed (18 weeks). Markers of diabetes including blood glucose, insulin, polydipsia, polyuria, and weight loss were measured. Pathological alterations and oxidative damage in glomeruli were also determined. Changes in protein expression of the Nrf2 pathway, as well as transforming growth factor-β1 (TGF-β1), fibronectin (FN), collagen IV, and p21/WAF1Cip1 (p21) were analyzed. The molecular mechanisms of Nrf2-mediated protection were investigated in an in vitro model using human renal mesangial cells (HRMCs).

resultsSF or CA significantly attenuated common metabolic disorder symptoms associated with diabetes in Nrf2(+/+) but not in Nrf2(-/-) mice, indicating SF and CA function through specific activation of the Nrf2 pathway. Furthermore, SF or CA improved renal performance and minimized pathological alterations in the glomerulus of STZ-Nrf2(+/+) mice. Nrf2 activation reduced oxidative damage and suppressed the expression of TGF-β1, extracellular matrix proteins and p21 both in vivo and in HRMCs. In addition, Nrf2 activation reverted p21-mediated growth inhibition and hypertrophy of HRMCs under hyperglycemic conditions.

conclusionsWe provide experimental evidence indicating that dietary compounds targeting Nrf2 activation can be used therapeutically to improve metabolic disorder and relieve renal damage induced by diabetes.

Indexed as

AcroleinAnimalsCell ProliferationCells, CulturedCyclin-Dependent Kinase Inhibitor p21Diabetic NephropathiesDose-Response Relationship, DrugExtracellular Matrix ProteinsHumansIsothiocyanatesKidneyMesangial CellsMiceMice, Inbred C57BLMice, KnockoutNF-E2-Related Factor 2AcroleincinnamaldehydeCyclin-Dependent Kinase Inhibitor p21Extracellular Matrix ProteinsIsothiocyanatesNF-E2-Related Factor 2Reactive Oxygen SpeciesRNA, Small InterferingsulforaphaneSulfoxidesThiocyanatesTransforming Growth Factor beta1

Identifiers

PMID22025779
PMCPMC3198067
OpenAlexW2154111720

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.