Evidence map›Paper›PMID 35149956›Full record

ArticleBiological trace element research2022

Quercetin Attenuates Copper-Induced Apoptotic Cell Death and Endoplasmic Reticulum Stress in SH-SY5Y Cells by Autophagic Modulation.

Joyeeta Chakraborty, Sourav Pakrashi, Arpita Sarbajna, Moumita Dutta, Jaya Bandyopadhyay

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In one paragraph

Article in Biological trace element research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
5.5field-weighted citation impact, top 3% 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

23 citing papers in PubMed, 44 citations in OpenAlex.

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  4. The pathogenesis of liver fibrosis in Wilson's disease: hepatocyte injury and regulation mediated by copper metabolism dysregulation.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026
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  13. [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024
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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

5 authors at 3 institutions in 1 country.

Joyeeta ChakrabortyMaulana Abul Kalam Azad University of Technology, West Bengal, NH 12, Haringhata, 741249, West Bengal, India.
Sourav PakrashiMaulana Abul Kalam Azad University of Technology, West Bengal, NH 12, Haringhata, 741249, West Bengal, India.
Arpita SarbajnaDivision of Electron Microscopy, ICMR-National Institute of Cholera and Enteric Diseases (NICED), Beliaghata, Kolkata, West Bengal, 700010, India.
Moumita DuttaDivision of Electron Microscopy, ICMR-National Institute of Cholera and Enteric Diseases (NICED), Beliaghata, Kolkata, West Bengal, 700010, India.
Jaya BandyopadhyayMaulana Abul Kalam Azad University of Technology, West Bengal, NH 12, Haringhata, 741249, West Bengal, India. jaya.bandyopadhyay@makautwb.ac.in.ORCID http://orcid.org/0000-0003-3696-5667
Maulana Abul Kalam Azad University of Technology, West Bengal · INNational Institute of Cholera and Enteric Diseases · INSaha Institute of Nuclear Physics · IN

Funding

indian council of medical research Grant No.3/1/3/JRF-2013/HRD-10-40901university grants commission Grant No.F/17-164/2013/SA-1
6 · The paper itself

Abstract

An increase in anthropogenic activities results in metal contamination in the ecosystem which has proven to be a major health risk in humans, as they make entry into cellular organelles via agricultural products. Copper (Cu) is one such metal that acts as an essential cofactor for the activity of several enzymes, one being the cytochrome c oxidase. The increasing number of evidence suggests a substantial correlation of Cu overload with neurodegenerative disorders, including Parkinson's disease (PD). We aim to explore quercetin, a well-known polyphenol, as an alternative for combating Cu-induced toxicity in human neuroblastoma SH-SY5Y secondary cell lines. We observed that Cu increased intracellular reactive oxygen species (ROS) levels, triggered morphological deformities and condensation of nuclei, caused an imbalance in the mitochondrial membrane potential (MMP), and finally induced apoptotic cell deaths. We further investigated the effects of Cu in modulating the pro- and anti-apoptotic proteins, such as Bax, Bcl-2, etc. However, quercetin reversed these changes owing to its antioxidant and anti-apoptotic properties, resulting in autophagy induction as an outcome of upregulation of autophagosome-bound microtubules-associated protein light chain-3 (LC3II). Besides, we investigated the role of Cu in stimulating ER stress proteins, viz. PERK, CHOP, and the concomitant responses of quercetin in restoring the ER homeostasis in cellular organelles like mitochondria and ER, against Cu-induced toxic insults by modulating autophagic pathways. Overall, this research work proposes a remedial approach for Cu-mediated neurotoxicity through understanding the diverse molecular signaling inside a cell with an aim to develop effective therapeutics.

Indexed as

Endoplasmic Reticulum StressNeuroblastomaAntioxidantsApoptosisApoptosis Regulatory ProteinsAutophagybcl-2-Associated X ProteinCell Line, TumorCopperEcosystemElectron Transport Complex IVHeat-Shock ProteinsHumansPolyphenolsProto-Oncogene Proteins c-bcl-2QuercetinAntioxidantsApoptosis Regulatory Proteinsbcl-2-Associated X ProteinCopperElectron Transport Complex IVHeat-Shock ProteinsPolyphenolsProto-Oncogene Proteins c-bcl-2QuercetinReactive Oxygen SpeciesApoptosisAutophagyCopperER stressQuercetinα-Syn

Identifiers

PMID35149956
OpenAlexW4210949181

What OpenQuestion holds

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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.