Evidence map›Paper›PMID 38910236›Full record

ArticleJournal of nanobiotechnology2024

Cold exposure-induced plasma exosomes impair bone mass by inhibiting autophagy.

Li-Min Lei, Fu-Xing-Zi Li, Xiao Lin, Feng Xu, Su-Kang Shan, Bei Guo, Ming-Hui Zheng, Ke-Xin Tang, Yi Wang, Qiu-Shuang Xu and 12 more

Erratum issuedAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of nanobiotechnology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 11 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

11 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
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  10. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

22 authors.

Li-Min LeiNational Clinical Research Center for Metabolic Disease, Hunan Provincial Key Laboratory of Metabolic Bone Diseases, Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, China.
Fu-Xing-Zi LiNational Clinical Research Center for Metabolic Disease, Hunan Provincial Key Laboratory of Metabolic Bone Diseases, Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, China.
Xiao LinDepartment of Radiology, The Second Xiangya Hospital, Central South University, Changsha, China.
Feng XuNational Clinical Research Center for Metabolic Disease, Hunan Provincial Key Laboratory of Metabolic Bone Diseases, Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, China.
Su-Kang ShanNational Clinical Research Center for Metabolic Disease, Hunan Provincial Key Laboratory of Metabolic Bone Diseases, Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, China.
Bei GuoNational Clinical Research Center for Metabolic Disease, Hunan Provincial Key Laboratory of Metabolic Bone Diseases, Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, China.
Ming-Hui ZhengNational Clinical Research Center for Metabolic Disease, Hunan Provincial Key Laboratory of Metabolic Bone Diseases, Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, China.
Ke-Xin TangNational Clinical Research Center for Metabolic Disease, Hunan Provincial Key Laboratory of Metabolic Bone Diseases, Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, China.
Yi WangNational Clinical Research Center for Metabolic Disease, Hunan Provincial Key Laboratory of Metabolic Bone Diseases, Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, China.
Qiu-Shuang XuNational Clinical Research Center for Metabolic Disease, Hunan Provincial Key Laboratory of Metabolic Bone Diseases, Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, China.
Wen-Lu OuyangNational Clinical Research Center for Metabolic Disease, Hunan Provincial Key Laboratory of Metabolic Bone Diseases, Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, China.
Jia-Yue DuanNational Clinical Research Center for Metabolic Disease, Hunan Provincial Key Laboratory of Metabolic Bone Diseases, Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, China.
Yun-Yun WuNational Clinical Research Center for Metabolic Disease, Hunan Provincial Key Laboratory of Metabolic Bone Diseases, Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, China.
Ye-Chi CaoNational Clinical Research Center for Metabolic Disease, Hunan Provincial Key Laboratory of Metabolic Bone Diseases, Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, China.
Zhi-Ang ZhouDepartment of Cardiovascular Surgery, the Second Xiangya Hospital, Central South University, Changsha, China.
Si-Yang HeNational Clinical Research Center for Metabolic Disease, Hunan Provincial Key Laboratory of Metabolic Bone Diseases, Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, China.
Yan-Lin WuNational Clinical Research Center for Metabolic Disease, Hunan Provincial Key Laboratory of Metabolic Bone Diseases, Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, China.
Xi ChenNational Clinical Research Center for Metabolic Disease, Hunan Provincial Key Laboratory of Metabolic Bone Diseases, Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, China.
Zheng-Jun LinDepartment of Orthopaedics, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China.
Yi PanDepartment of Endocrinology, The Second Affiliated Hospital of Kunming Medical University, No. 374 The Dianmian Avenue, Wuhua, Kunming, Yunnan, 650101, China.
Ling-Qing YuanNational Clinical Research Center for Metabolic Disease, Hunan Provincial Key Laboratory of Metabolic Bone Diseases, Department of Metabolism and Endocrinology, The Second Xiangya Hospital, Central South University, Changsha, China. allenylq@csu.edu.cn.
Zhi-Hong LiDepartment of Orthopaedics, The Second Xiangya Hospital, Central South University, Changsha, Hunan, 410011, China. lizhihong@csu.edu.cn.

Funding

Health Research Project of Hunan Provincial Health Commission W20243019Kunming medicine joint special project 202001AY070001-222National Clinical Key Specialties Major Research Projects Z2023026National Key Research & Development Program No. 2021YFC2501701, 2023YFC2507600National Natural Science Foundation of China No. 82370892, 82070910, 82100944, 82200869 and 82100494National Undergraduate Innovation Training Program of Central South University 2022105330213 and 2022105330235The Health Research Project in Hunan Province No. 20231696, 202103062278the Natural Science Foundation of Hunan Province No. 2022JJ40721, 2022JJ40715
6 · The paper itself

Abstract

Recently, environmental temperature has been shown to regulate bone homeostasis. However, the mechanisms by which cold exposure affects bone mass remain unclear. In our present study, we observed that exposure to cold temperature (CT) decreased bone mass and quality in mice. Furthermore, a transplant of exosomes derived from the plasma of mice exposed to cold temperature (CT-EXO) can also impair the osteogenic differentiation of BMSCs and decrease bone mass by inhibiting autophagic activity. Rapamycin, a potent inducer of autophagy, can reverse cold exposure or CT-EXO-induced bone loss. Microarray sequencing revealed that cold exposure increases the miR-25-3p level in CT-EXO. Mechanistic studies showed that miR-25-3p can inhibit the osteogenic differentiation and autophagic activity of BMSCs. It is shown that inhibition of exosomes release or downregulation of miR-25-3p level can suppress CT-induced bone loss. This study identifies that CT-EXO mediates CT-induced osteoporotic effects through miR-25-3p by inhibiting autophagy via targeting SATB2, presenting a novel mechanism underlying the effect of cold temperature on bone mass.

Indexed as

AutophagyCold TemperatureExosomesMice, Inbred C57BLMicroRNAsOsteogenesisAnimalsBone and BonesBone DensityCell DifferentiationFemaleMesenchymal Stem CellsMiceOsteoporosisSirolimusMicroRNAsSirolimusAutophagyBone massCold exposureExosomesmiR-25-3pOsteogenesis

Identifiers

PMID38910236
PMCPMC11194967

What Socratic holds

Textmetadata
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 Socratic graph.