Evidence map›Paper›PMID 33432550›Full record

ArticleCell biochemistry and biophysics2021

CLIC1 Inhibition Protects Against Cellular Senescence and Endothelial Dysfunction Via the Nrf2/HO-1 Pathway.

Dezhao Lu, Yifei Le, Jiali Ding, Xiaobing Dou, Wei Mao, Ji Zhu

Abstract read
PubMed Publisher
In one paragraph

Article in Cell biochemistry and biophysics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

13 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Cellular and molecular mechanisms underlying cardiovascular aging.Cellular & molecular biology letters · 2025
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Effects of Pterostilbene on Cardiovascular Health and Disease.Current issues in molecular biology · 2024
    Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
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

6 authors at 2 institutions in 1 country.

Dezhao LuCollege of Life Science, Zhejiang Chinese Medical University, 310053, Hangzhou, China.ORCID http://orcid.org/0000-0001-5227-6445
Yifei LeCollege of Life Science, Zhejiang Chinese Medical University, 310053, Hangzhou, China.ORCID http://orcid.org/0000-0002-4164-4983
Jiali DingCollege of Life Science, Zhejiang Chinese Medical University, 310053, Hangzhou, China.ORCID http://orcid.org/0000-0003-0040-8439
Xiaobing DouCollege of Life Science, Zhejiang Chinese Medical University, 310053, Hangzhou, China.ORCID http://orcid.org/0000-0003-1994-2770
Wei MaoCardiovascular department, The First Affiliated Hospital of Zhejiang Chinese Medicine University, 310006, Hangzhou, China. maoweilw@163.com.ORCID http://orcid.org/0000-0002-2465-3079
Ji ZhuClinical Laboratory, The Third Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, China. zhuji1982@163.com.ORCID http://orcid.org/0000-0001-7678-740X
Zhejiang Chinese Medical University · CNThe Third Affiliated Hospital of Zhejiang Chinese Medical University · CN

Funding

Natural Science Foundation of Zhejiang Province LY19H280003the Key Laboratory of Integrative Chinese and Western Medicine for the Diagnosis and Treatment of Circulatory Diseases of Zhejiang Province 2C32005
6 · The paper itself

Abstract

Chloride intracellular channel 1 (CLIC1) is a sensor of oxidative stress in endothelial cells (EC). However, the mechanism by which CLIC1 mediate the regulation of endothelial dysfunction has not been established. In this study, overexpressed CLIC1 impaired the ability of the vascular cells to resist oxidative damage and promoted cellular senescence. Besides, suppressed CLIC1 protected against cellular senescence and dysfunction in Human Umbilical Vein Endothelial Cells (HUVECs) through the Nrf2/HO-1 pathway. We also found that ROS-activated CLIC1-induced oxidative stress in HUVECs. Nrf2 nuclear translocation was inhibited by CLIC1 overexpression, but was enhanced by IAA94 (CLICs inhibitor) treatment or knockdown of CLIC1. The Nrf2/HO-1 pathway plays a critical role in the anti-oxidative effect of suppressing CLIC1. And inhibition of CLIC1 decreases oxidative stress injury by downregulating the levels of ROS, MDA, and the expression of EC effectors (ICAM1 and VCAM1) protein expression and promotes the activity of superoxide dismutase (SOD). The AMPK-mediated signaling pathway activates Nrf2 through Nrf2 phosphorylation and nuclear translocation, which is also regulated by CLIC1. Moreover, the activation of CLIC1 contributes to H

Indexed as

Cellular SenescenceSignal TransductionAcetylcysteineChloride ChannelsHeme Oxygenase-1HumansHuman Umbilical Vein Endothelial CellsHydrogen PeroxideIntercellular Adhesion Molecule-1MitochondriaMitochondrial DynamicsNF-E2-Related Factor 2Oxidative StressReactive Oxygen SpeciesRNA InterferenceRNA, Small InterferingAcetylcysteineChloride ChannelsCLIC1 protein, humanHeme Oxygenase-1Hydrogen PeroxideIntercellular Adhesion Molecule-1NF-E2-Related Factor 2Reactive Oxygen SpeciesRNA, Small InterferingSuperoxide DismutaseVascular Cell Adhesion Molecule-1CLIC1Endothelial dysfunctionHUVECsNrf2Oxidative stress

Identifiers

PMID33432550
OpenAlexW3119461017

What OpenQuestion holds

Textmetadata
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.