Evidence map›Paper›PMID 38245790›Full record

ArticleJournal of translational medicine2024

(+)-Lipoic acid reduces mitochondrial unfolded protein response and attenuates oxidative stress and aging in an in vitro model of non-alcoholic fatty liver disease.

Lucia Longhitano, Alfio Distefano, Nicolò Musso, Paolo Bonacci, Laura Orlando, Sebastiano Giallongo, Daniele Tibullo, Simona Denaro, Giuseppe Lazzarino, Jessica Ferrigno and 10 more

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
5.8field-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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

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  12. [Potential of early diagnosis and targeted therapy for Klotho protein in chronic kidney disease].Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025
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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

20 authors at 4 institutions in 2 countries.

Lucia Longhitano *Department of Biomedical and Biotechnological Sciences, University of Catania, 95123, Catania, Italy.
Alfio Distefano *Department of Biomedical and Biotechnological Sciences, University of Catania, 95123, Catania, Italy.
Nicolò MussoDepartment of Biomedical and Biotechnological Sciences, University of Catania, 95123, Catania, Italy.
Paolo BonacciDepartment of Biomedical and Biotechnological Sciences, University of Catania, 95123, Catania, Italy.
Laura OrlandoDepartment of Biomedical and Biotechnological Sciences, University of Catania, 95123, Catania, Italy.
Sebastiano GiallongoDepartment of Biomedical and Biotechnological Sciences, University of Catania, 95123, Catania, Italy.
Daniele TibulloDepartment of Biomedical and Biotechnological Sciences, University of Catania, 95123, Catania, Italy.
Simona DenaroDepartment of Biomedical and Biotechnological Sciences, University of Catania, 95123, Catania, Italy.
Giuseppe LazzarinoDepartment of Biomedical and Biotechnological Sciences, University of Catania, 95123, Catania, Italy.
Jessica FerrignoDepartment of Biomedical and Biotechnological Sciences, University of Catania, 95123, Catania, Italy.
Anna NicolosiHospital Pharmacy Unit, Ospedale Cannizzaro, 95125, Catania, Italy.
Amer M AlanaziPharmaceutical Biotechnology Laboratory, Department of Pharmaceutical Chemistry, College of Pharmacy, King Saud University, 11451, Riyadh, Saudi Arabia.
Federico SalomoneDivision of Gastroenterology, Ospedale Di Acireale, Azienda Sanitaria Provinciale Di Catania, Catania, Italy.
Emanuela TropeaDepartment of Biomedical and Biotechnological Sciences, University of Catania, 95123, Catania, Italy.
Ignazio Alberto BarbagalloDepartment of Biomedical and Biotechnological Sciences, University of Catania, 95123, Catania, Italy.
Vincenzo BramantiU.O.S. Laboratory Analysis, Maggiore "Nino Baglieri" Hospital - ASP Ragusa, 97015, Modica (RG), Italy.
Giovanni Li VoltiDepartment of Biomedical and Biotechnological Sciences, University of Catania, 95123, Catania, Italy. livolti@unict.it.ORCID 0000-0002-8678-2183
Giacomo LazzarinoUniCamillus-Saint Camillus International University of Health Sciences, Via Di Sant'Alessandro 8, 00131, Rome, Italy.
Daniele TorellaDepartment of Experimental and Clinical Medicine, Magna Graecia University, Catanzaro, Italy.
Angela Maria AmoriniDepartment of Biomedical and Biotechnological Sciences, University of Catania, 95123, Catania, Italy.
University of Catania · ITKing Saud University · SAMagna Graecia University · ITOspedale Cannizzaro · IT

Funding

King Saud University, Riyadh, Saudi Arabia RSP2024R261University of catania PIACERI 2020-2022 IMYTRA
6 · The paper itself

Abstract

backgroundNon-alcoholic fatty liver disease (NAFLD) is a liver disorder characterized by the ac-cumulation of fat in hepatocytes without alcohol consumption. Mitochondrial dysfunction and endoplasmic reticulum (ER) stress play significant roles in NAFLD pathogenesis. The unfolded protein response in mitochondria (UPRmt) is an adaptive mechanism that aims to restore mitochondrial protein homeostasis and mitigate cellular stress. This study aimed to investigate the effects of ( +)-Lipoic acid (ALA) on UPRmt, inflammation, and oxidative stress in an in vitro model of NAFLD using HepG2 cells treated with palmitic acid and oleic acid to induce steatosis.

resultsTreatment with palmitic and oleic acids increased UPRmt-related proteins HSP90 and HSP60 (heat shock protein), and decreased CLPP (caseinolytic protease P), indicating ER stress activation. ALA treatment at 1 μM and 5 μM restored UPRmt-related protein levels. PA:OA (palmitic acid:oleic acid)-induced ER stress markers IRE1α (Inositol requiring enzyme-1), CHOP (C/EBP Homologous Protein), BIP (Binding Immunoglobulin Protein), and BAX (Bcl-2-associated X protein) were significantly reduced by ALA treatment. ALA also enhanced ER-mediated protein glycosylation and reduced oxidative stress, as evidenced by decreased GPX1 (Glutathione peroxidase 1), GSTP1 (glutathione S-transferase pi 1), and GSR (glutathione-disulfide reductase) expression and increased GSH (Glutathione) levels, and improved cellular senescence as shown by the markers β-galactosidase, γH2Ax and Klotho-beta.

conclusionsIn conclusion, ALA ameliorated ER stress, oxidative stress, and inflammation in HepG2 cells treated with palmitic and oleic acids, potentially offering therapeutic benefits for NAFLD providing a possible biochemical mechanism underlying ALA beneficial effects.

Indexed as

Non-alcoholic Fatty Liver DiseaseThioctic AcidCellular SenescenceEndoplasmic Reticulum StressEndoribonucleasesHepatocytesHumansInflammationLiverOleic AcidOxidative StressPalmitic AcidPalmitic AcidsProtein Serine-Threonine KinasesUnfolded Protein ResponseEndoribonucleasesOleic AcidPalmitic AcidPalmitic AcidsProtein Serine-Threonine KinasesThioctic AcidMitochondrial dysfunctionNon-alcoholic fatty liver diseaseOxidative stressUnfolded protein re-sponse

Identifiers

PMID38245790
PMCPMC10799515
OpenAlexW4391051358

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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.