Evidence map›Paper›PMID 37365870›Full record

ArticleActa biochimica et biophysica Sinica2023

Galangin mitigates glucocorticoid-induced osteoporosis by activating autophagy of BMSCs via triggering the PKA/CREB signaling pathway.

Chenying Zeng, Shan Wang, Huimin Gu, Fenglei Chen, Ziming Wang, Jinteng Li, Zhongyu Xie, Pei Feng, Huiyong Shen, Yanfeng Wu

Open access · diamondAbstract read
In one paragraph

Article in Acta biochimica et biophysica Sinica, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

17 citing papers in PubMed, 23 citations in OpenAlex.

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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

10 authors at 1 institution in 1 country.

Chenying ZengCenter for Biotherapy, Eighth Affiliated Hospital of Sun Yat-sen University, Shenzhen 518033, China.
Shan WangCenter for Biotherapy, Eighth Affiliated Hospital of Sun Yat-sen University, Shenzhen 518033, China.
Huimin GuCenter for Biotherapy, Eighth Affiliated Hospital of Sun Yat-sen University, Shenzhen 518033, China.
Fenglei ChenDepartment of Orthopedics, Eighth Affiliated Hospital of Sun Yat-sen University, Shenzhen 518033, China.
Ziming WangDepartment of Orthopedics, Eighth Affiliated Hospital of Sun Yat-sen University, Shenzhen 518033, China.
Jinteng LiDepartment of Orthopedics, Eighth Affiliated Hospital of Sun Yat-sen University, Shenzhen 518033, China.
Zhongyu XieDepartment of Orthopedics, Eighth Affiliated Hospital of Sun Yat-sen University, Shenzhen 518033, China.
Pei FengCenter for Biotherapy, Eighth Affiliated Hospital of Sun Yat-sen University, Shenzhen 518033, China.
Huiyong ShenDepartment of Orthopedics, Eighth Affiliated Hospital of Sun Yat-sen University, Shenzhen 518033, China.
Yanfeng WuCenter for Biotherapy, Eighth Affiliated Hospital of Sun Yat-sen University, Shenzhen 518033, China.
Sun Yat-sen Memorial Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glucocorticoid-induced osteoporosis (GIOP), one of the most common and serious adverse effects associated with glucocorticoid administration, manifests as decreased bone formation and increased bone resorption, eventually culminating in bone loss. Galangin (GAL) is a flavonoid extracted from the medicinal herbal galangal that possesses a variety of pharmacological activities and can inhibit osteoclastogenesis. However, the effects of GAL on GIOP remain unclear. Our study aims to explore the effects of GAL on GIOP in mice and the underlying mechanism. Our results show that GAL markedly mitigates the severity of dexamethasone (Dex)-induced osteoporosis in mice and potentiates osteogenic differentiation in mouse bone marrow-derived mesenchymal stem cells (BMSCs). Furthermore, GAL also significantly counteracts Dex-mediated suppression of osteogenic differentiation and autophagy in human BMSCs. GAL augments PKA/CREB-mediated autophagic flux in BMSCs and the bones of osteoporotic mice. GAL-mediated osteogenic differentiation in Dex-treated BMSCs is significantly decreased by the PKA inhibitor H89 and autophagy inhibitor 3-methyladenine. Collectively, our data indicate that GAL can ameliorate GIOP, partly by augmenting the mineralization of BMSCs by potentiating PKA/CREB-mediated autophagic flux, highlighting its potential therapeutic use in treating glucocorticoid-related osteoporosis.

Indexed as

GlucocorticoidsOsteoporosisAnimalsAutophagyCell DifferentiationFlavonoidsHumansMiceOsteogenesisSignal TransductionFlavonoidsgalanginGlucocorticoidsautophagyBMSCdexamethasonegalanginglucocorticoid-induced osteoporosis

Identifiers

PMID37365870
PMCPMC10448057
OpenAlexW4362574958

What OpenQuestion holds

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LicenceCC BY
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.