Evidence map›Paper›PMID 29427075›Full record

ReviewCellular and molecular life sciences : CMLS2018

Autophagy as a target for glucocorticoid-induced osteoporosis therapy.

Gengyang Shen, Hui Ren, Qi Shang, Ting Qiu, Xiang Yu, Zhida Zhang, Jinjing Huang, Wenhua Zhao, Yuzhuo Zhang, De Liang and 1 more

Open access · greenAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
7.9field-weighted citation impact, top 2% 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

40 citing papers in PubMed, 76 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

11 authors at 2 institutions in 1 country.

Gengyang ShenGuangzhou University of Chinese Medicine, Guangzhou, 510405, China.
Hui RenDepartment of Spinal Surgery, The First Affiliated Hospital, Guangzhou University of Chinese Medicine, Guangzhou, 510405, China.
Qi ShangGuangzhou University of Chinese Medicine, Guangzhou, 510405, China.
Ting QiuGuangzhou University of Chinese Medicine, Guangzhou, 510405, China.
Xiang YuGuangzhou University of Chinese Medicine, Guangzhou, 510405, China.
Zhida ZhangGuangzhou University of Chinese Medicine, Guangzhou, 510405, China.
Jinjing HuangGuangzhou University of Chinese Medicine, Guangzhou, 510405, China.
Wenhua ZhaoGuangzhou University of Chinese Medicine, Guangzhou, 510405, China.
Yuzhuo ZhangGuangzhou University of Chinese Medicine, Guangzhou, 510405, China.
De LiangDepartment of Spinal Surgery, The First Affiliated Hospital, Guangzhou University of Chinese Medicine, Guangzhou, 510405, China.
Xiaobing JiangDepartment of Spinal Surgery, The First Affiliated Hospital, Guangzhou University of Chinese Medicine, Guangzhou, 510405, China. spinedrjxb@sina.com.ORCID http://orcid.org/0000-0002-8009-0282
Guangzhou University of Chinese Medicine · CNFirst Affiliated Hospital of Guangzhou University of Chinese Medicine · CN

Funding

Excellent Doctor Project of the First School of Clinic Medicine of Guangzhou University of Chinese Medicine YB201501Excellent Doctor Project of the First School of Clinic Medicine of Guangzhou University of Chinese Medicine YB201602National Natural Science Foundation of China (CN) 81674000Natural Science Foundation of China 81503591Natural Science Foundation of China 81774338Natural Science Foundation of Guangdong Province 2014A030310082Science and Technology Projects of Guangdong Province 2014A020221021Science and Technology Projects of Guangdong Province 2016A020226006
6 · The paper itself

Abstract

Autophagy takes part in regulating the eukaryotic cells function and the progression of numerous diseases, but its clinical utility has not been fully developed yet. Recently, mounting evidences highlight an important correlation between autophagy and bone homeostasis, mediated by osteoclasts, osteocytes, bone marrow mesenchymal stem cells, and osteoblasts, and autophagy plays a vital role in the pathogenesis of glucocorticoid-induced osteoporosis (GIOP). The combinations of autophagy activators/inhibitors with anti-GIOP first-line drugs or some new autophagy-based manipulators, such as regulation of B cell lymphoma 2 family proteins and caspase-dependent clearance of autophagy-related gene proteins, are likely to be the promising approaches for GIOP clinical treatments. In view of the important role of autophagy in the pathogenesis of GIOP, here we review the potential mechanisms about the impacts of autophagy in GIOP and its association with GIOP therapy.

Indexed as

AutophagyBone and BonesBone Density Conservation AgentsCalciumGlucocorticoidsHomeostasisHumansOsteogenesisOsteoporosisBone Density Conservation AgentsCalciumGlucocorticoidsApoptosisAutophagyBone metabolic diseasesGlucocorticoid-induced osteoporosisReviewTherapeutic target

Identifiers

PMID29427075
PMCPMC11105583
OpenAlexW2792643378

What OpenQuestion holds

Textmetadata
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.