Evidence map›Paper›PMID 35304586›Full record

ArticleScientific reports2022

L-Carnitine reduces reactive oxygen species/endoplasmic reticulum stress and maintains mitochondrial function during autophagy-mediated cell apoptosis in perfluorooctanesulfonate-treated renal tubular cells.

Yuan-Chii Gladys Lee, Hsiu-Chu Chou, Yen-Ting Chen, Szu-Yu Tung, Tsui-Ling Ko, Batsaikhan Buyandelger, Li-Li Wen, Shu-Hui Juan

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

19 citing papers in PubMed, 38 citations in OpenAlex.

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  18. Oxygen is toxic in the cold inFrontiers in physiology · 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

8 authors at 3 institutions in 1 country.

Yuan-Chii Gladys LeeGraduate Institute of Biomedical Informatics, College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan.
Hsiu-Chu ChouDepartment of Anatomy and Cell Biology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Yen-Ting ChenDepartment of Physiology, School of Medicine, College of Medicine, Taipei Medical University, 250 Wu-Hsing Street, Taipei, 110, Taiwan.
Szu-Yu TungDepartment of Physiology, School of Medicine, College of Medicine, Taipei Medical University, 250 Wu-Hsing Street, Taipei, 110, Taiwan.
Tsui-Ling KoCollege of Science, National Sun Yat-Sen University, Kaohsiung, Taiwan.
Batsaikhan BuyandelgerDepartment of Physiology, School of Medicine, College of Medicine, Taipei Medical University, 250 Wu-Hsing Street, Taipei, 110, Taiwan.
Li-Li WenDepartment of Clinical Laboratory, En Chu Kong Hospital, New Taipei City, 237, Taiwan.
Shu-Hui JuanDepartment of Physiology, School of Medicine, College of Medicine, Taipei Medical University, 250 Wu-Hsing Street, Taipei, 110, Taiwan. juansh@tmu.edu.tw.
Taipei Medical University · TWEn Chu Kong Hospital · TWNational Sun Yat-sen University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We previously reported that perfluorooctanesulfonate (PFOS) causes autophagy-induced apoptosis in renal tubular cells (RTCs) through a mechanism dependent on reactive oxygen species (ROS)/extracellular signal-regulated kinase. This study extended our findings and determined the therapeutic potency of L-Carnitine in PFOS-treated RTCs. L-Carnitine (10 mM) reversed the effects of PFOS (100 µM) on autophagy induction and impaired autophagy flux. Furthermore, it downregulated the protein level of p47Phox, which is partly related to PFOS-induced increased cytosolic ROS in RTCs. Moreover, L-Carnitine reduced ROS production in mitochondria and restored PFOS-impeded mitochondrial function, leading to sustained normal adenosine triphosphate synthesis and oxygen consumption and reduced proton leakage in a Seahorse XF stress test. The increased inositol-requiring enzyme 1α expression by PFOS, which indicated endoplasmic reticulum (ER) stress activation, was associated with PFOS-mediated autophagy activation that could be attenuated through 4-phenylbutyrate (5 mM, an ER stress inhibitor) and L-Carnitine pretreatment. Therefore, by reducing the level of IRE1α, L-Carnitine reduced the levels of Beclin and LC3BII, consequently reducing the level of apoptotic biomarkers including Bax and cleaving PARP and caspase 3. Collectively, these results indicate that through the elimination of oxidative stress, extracellular signal-regulated kinase activation, and ER stress, L-Carnitine reduced cell autophagy/apoptosis and concomitantly increased cell viability in RTCs. This study clarified the potential mechanism of PFOS-mediated RTC apoptosis and provided a new strategy for using L-Carnitine to prevent and treat PFOS-induced RTC apoptosis.

Indexed as

Endoplasmic Reticulum StressEndoribonucleasesAlkanesulfonic AcidsApoptosisAutophagyCarnitineExtracellular Signal-Regulated MAP KinasesFluorocarbonsMitochondriaProtein Serine-Threonine KinasesReactive Oxygen SpeciesAlkanesulfonic AcidsCarnitineEndoribonucleasesExtracellular Signal-Regulated MAP KinasesFluorocarbonsperfluorooctane sulfonic acidProtein Serine-Threonine KinasesReactive Oxygen Species

Identifiers

PMID35304586
PMCPMC8933466
OpenAlexW4220706896

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.