Evidence map›Paper›PMID 34609092›Full record

ArticleJournal of Korean medical science2021

Spironolactone Attenuates Methylglyoxal-induced Cellular Dysfunction in MC3T3-E1 Osteoblastic Cells.

So Young Park, Kwang Sik Suh, Woon-Won Jung, Sang Ouk Chin

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of Korean medical science, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

6 citing papers in PubMed, 8 citations in OpenAlex.

  1. Effects of spironolactone on cytotoxic damage in osteoblasts.Experimental and therapeutic medicine · 2026
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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 3 institutions in 1 country.

So Young ParkDepartment of Endocrinology and Metabolism, Kyung Hee University Hospital, Seoul, Korea.ORCID https://orcid.org/0000-0002-4820-9415
Kwang Sik SuhDepartment of Endocrinology and Metabolism, Kyung Hee University School of Medicine, Seoul, Korea.ORCID https://orcid.org/0000-0002-2942-7601
Woon-Won JungDepartment of Biomedical Laboratory Science, College of Health and Medical Sciences, Cheongju University, Cheongju, Korea.ORCID https://orcid.org/0000-0002-7013-5993
Sang Ouk ChinDepartment of Endocrinology and Metabolism, Kyung Hee University Hospital, Seoul, Korea.ORCID https://orcid.org/0000-0001-5914-3653
Kyung Hee University · KRCheongju University · KRKyung Hee University Dental Hospital · KR

Funding

Kyung Hee University KHU-20182181National Research Foundation of Korea NRF-2019R1G1A1099081
6 · The paper itself

Abstract

backgroundMethylglyoxal (MG) is associated with the pathogenesis of age- and diabetes-related complications. Spironolactone is a competitive antagonist of aldosterone that is widely employed in the treatment of hypertension and heart failure. This study examined the effects of spironolactone on MG-induced cellular dysfunction in MC3T3-E1 osteoblastic cells.

methodsMC3T3-E1 cells were treated with spironolactone in the presence of MG. The mitochondrial function, bone formation activity, oxidative damage, inflammatory cytokines, glyoxalase I activity, and glutathione (GSH) were measured.

resultsPretreatment of MC3T3-E1 osteoblastic cells with spironolactone prevented MG-induced cell death, and improved bone formation activity. Spironolactone reduced MG-induced endoplasmic reticulum stress, production of intracellular reactive oxygen species, mitochondrial superoxides, cardiolipin peroxidation, and inflammatory cytokines. Pretreatment with spironolactone also increased the level of reduced GSH and the activity of glyoxalase I. MG induced mitochondrial dysfunction, but markers of mitochondrial biogenesis such as mitochondrial membrane potential, adenosine triphosphate, proliferator-activated receptor gamma coactivator 1α, and nitric oxide were significantly improved by treatment of spironolactone.

conclusionSpironolactone could prevent MG-induced cytotoxicity in MC3T3-E1 osteoblastic cells by reduction of oxidative stress. The oxidative stress reduction was explained by spironolactone's inhibition of advanced glycation end-product formation, restoring mitochondrial dysfunction, and anti-inflammatory effect.

Indexed as

AnimalsApoptosisCell DifferentiationCell LineCytokinesEndoplasmic Reticulum StressGlutathioneGlycation End Products, AdvancedLactoylglutathione LyaseMembrane Potential, MitochondrialMiceNitric OxideOsteoblastsOxidative StressProtective AgentsPyruvaldehydeCytokinesGlutathioneGlycation End Products, AdvancedLactoylglutathione LyaseNitric OxideProtective AgentsPyruvaldehydeReactive Oxygen SpeciesSpironolactoneAdvanced Glycation End ProductsAntioxidantsMitochondriaOsteoblastsSpironolactone

Identifiers

PMID34609092
PMCPMC8490790
OpenAlexW3200344384

What OpenQuestion holds

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LicenceCC BY-NC
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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.