Evidence map›Paper›PMID 33070655›Full record

ArticleClinical and experimental hypertension (New York, N.Y. : 1993)2021

Nrf2 inhibition induces oxidative stress, renal inflammation and hypertension in mice.

Zeba Farooqui, Razia Sultana Mohammad, Mustafa F Lokhandwala, Anees Ahmad Banday

Open access · greenAbstract read
In one paragraph

Article in Clinical and experimental hypertension (New York, N.Y. : 1993), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 10% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
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  15. NRF2 in kidney physiology and disease.Physiological reports · 2024
    Review
  16. Anti-Inflammatory Effects of Peripheral Dopamine.International journal of molecular sciences · 2023
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Zeba FarooquiHeart and Kidney Institute, College of Pharmacy, University of Houston , Houston, Texas, USA.
Razia Sultana MohammadHeart and Kidney Institute, College of Pharmacy, University of Houston , Houston, Texas, USA.
Mustafa F LokhandwalaHeart and Kidney Institute, College of Pharmacy, University of Houston , Houston, Texas, USA.
Anees Ahmad BandayHeart and Kidney Institute, College of Pharmacy, University of Houston , Houston, Texas, USA.
University of Houston · US

Funding

Renal Dopamine D1 Receptor Function during Oxidative Stress-related HypertensionR01HL139808 · NHLBI · UNIVERSITY OF HOUSTON · PI BANDAY, ANEES AHMAD · 2018 to 2021
$2.6M
NHLBI NIH HHS R01 HL139808
6 · The paper itself

Abstract

Oxidative stress and renal inflammation play a pivotal role in the pathogenesis of hypertension. The redox-sensitive transcription factor, nuclear factor E2-related factor 2 (Nrf2) is the master regulator of phase II antioxidant enzymes that protects against oxidative stress and inflammation. This study aimed to investigate the effect of Nrf2 inhibition on oxidative stress-associated hypertension and renal dopamine 1 receptor (D1R) dysfunction in mice. Male C57BL/6 J mice were treated with a pro-oxidant, L-buthionine sulfoximine (BSO) (10 mmol/L in drinking water), and ML385 (10 kg body weight/kg body weight/day, intraperitoneally), a novel Nrf2 inhibitor that blocks Nrf2 regulated downstream target genes expression. Mice treated with BSO exhibited oxidative stress, renal functional impairment, inflammation, and elevated blood pressure. Also, BSO treatment increased the activity of phase II antioxidant enzyme, NAD(P)H: quinone oxidoreductase-1 (NQO-1). BSO and ML385 co-treatment exhibited a robust increase in blood pressure, oxidative stress and intensified the renal function deterioration as indicated by a significant increase in serum creatinine, urinary albumin excretion rate, and albumin to creatinine ratio and decreased glomerular filtration rate (GFR). Also, BSO and ML385 co-treatment downregulated NQO-1 and significantly altered the inflammatory cytokines, IL-1β and IL-10 levels. A D1R agonist SKF38393 failed to promote urinary sodium excretion indicating functional impairment in renal D1R. ML385 per se did not affect mean arterial pressure, GFR, and renal D1R function. Taken together, we concluded that the Nrf2 inhibition aggravated oxidative stress and inflammation by diminishing phase II antioxidant defense that deteriorates renal function and contributes to the development of hypertension in mice.

Indexed as

HypertensionNF-E2-Related Factor 2Reactive Oxygen SpeciesAnimalsAntioxidantsBlood PressureButhionine SulfoximineEnzyme InhibitorsGene Expression RegulationInflammationKidneyMaleMiceMice, Inbred C57BLOxidative StressAntioxidantsButhionine SulfoximineEnzyme InhibitorsNfe2l2 protein, mouseNF-E2-Related Factor 2Reactive Oxygen SpecieshypertensioninflammationML385NRF2Oxidative stress

Identifiers

PMID33070655
PMCPMC7790982
OpenAlexW3093438035

What OpenQuestion holds

Textmetadata
LicenceTDM
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.