Evidence map›Paper›PMID 41259452›Full record

ArticleBrazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica2025

H2S inhibits high glucose-induced osteoblast injury by inhibiting ferroptosis in diabetic osteoporosis in vitro.

Qingping Shi, Feihong Chen, Wen Wu

Abstract read
In one paragraph

Article in Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. 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

3 authors.

Qingping ShiDepartment of Endocrinology, Guangdong Geriatrics Institute, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China.ORCID http://orcid.org/0009-0001-7256-5110
Feihong ChenDepartment of Respiratory Medicine, People's Hospital of Shenzhen Baoan District, The Second Affiliated Hospital of Shenzhen University, Shenzhen, China.ORCID http://orcid.org/0009-0001-8137-1342
Wen WuDepartment of Endocrinology, Guangdong Geriatrics Institute, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China.ORCID http://orcid.org/0000-0002-2144-8491

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic osteoporosis (DOP) is a complication of prolonged hyperglycemia. Hydrogen sulfide (H2S) has been identified as a protective factor in bone development. However, the mechanism by which H2S antagonizes the effects of high glucose (HG) on osteoblasts remains unclear. The effects of HG and H2S on osteoblasts were assessed through transcriptomic and metabolomic sequencing to identify key changes in gene expression and metabolism. Reactive oxygen species (ROS) levels, mitochondrial membrane potential (MMP), alkaline phosphatase (ALP) activity, mineralization, iron ion levels, malondialdehyde (MDA) levels, cell proliferation, and protein expression were evaluated. Transcriptomic analysis revealed significant upregulation of the ferroptosis pathway in HG-treated osteoblasts. Fer-1 and H2S antagonized the HG-induced decrease in osteoblast cell proliferation, increase in ROS production, decrease in MMP, decrease in ALP, decrease in mineralized nodules, and increase in iron ions and MDA. Transcriptome analysis showed Fer-1 was involved in upregulating the synthesis, secretion, and action of parathyroid hormone and estrogen synthesis, while downregulating the mitogen-activated protein kinases (MAPK) pathway. Metabolomic analysis showed H2S restored glutathione metabolism, reducing pyroglutamic acid and L-5-oxoproline levels. Transcriptome sequencing identified downregulated genes (hmox1, ncoa4) and an upregulated gene (slc40a1) related to ferroptosis in the H2S + HG group compared with the HG group. Western blot analysis indicated H2S increased GPX4 and SLC7A11 levels while reducing ACSL4 expression compared with the HG group. Ferroptosis may be involved in the pathogenesis of DOP and H2S can effectively alleviate osteoblast injury by inhibiting ferroptosis in DOP.

Indexed as

Diabetes ComplicationsFerroptosisGlucoseHydrogen SulfideOsteoblastsOsteoporosisAnimalsCell ProliferationReactive Oxygen SpeciesGlucoseHydrogen SulfideReactive Oxygen Species

Identifiers

PMID41259452
PMCPMC12645440

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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.