Evidence map›Paper›PMID 39164234›Full record

ArticleBone research2024

Rejuvenation of BMSCs senescence by pharmacological enhancement of TFEB-mediated autophagy alleviates aged-related bone loss and extends lifespan in middle aged mice.

Ziwei Luo, Wanyi Wei, Dawei Qiu, Zixia Su, Liangpu Liu, Honghai Zhou, Hao Cui, Li Yang

Abstract read
In one paragraph

Article in Bone research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
–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

20 citing papers in PubMed.

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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

8 authors.

Ziwei Luo *College of Orthopedics, Guangxi University of Chinese Medicine, Nanning, 530200, Guangxi, China. luo.ziwei@live.cn.ORCID http://orcid.org/0000-0003-1208-7847
Wanyi Wei *Faculty of Chinese Medicine Science, Guangxi University of Chinese Medicine, Nanning, 530200, Guangxi, China.
Dawei QiuDepartment of Physical Education, Guangxi University of Chinese Medicine, Nanning, 530200, Guangxi, China.
Zixia SuGuangxi Key Laboratory of Efficacy Study on Chinese Materia Medica, Guangxi University of Chinese Medicine, Nanning, 530200, Guangxi, China.
Liangpu LiuCollege of Orthopedics, Guangxi University of Chinese Medicine, Nanning, 530200, Guangxi, China.
Honghai ZhouCollege of Orthopedics, Guangxi University of Chinese Medicine, Nanning, 530200, Guangxi, China.
Hao CuiCollege of Pharmacy, Guangxi University of Chinese Medicine, Nanning, 530200, Guangxi, China. ch008szx6@163.com.
Li YangKey Laboratory of Biorheological Science and Technology, Ministry of Education, Bioengineering College, Chongqing University, Chongqing, 400030, China.

Funding

Science and Technology Department of Guangxi Zhuang Autonomous (Guangxi Science and Technology Department) Guike AD19245094Science and Technology Department of Guangxi Zhuang Autonomous (Guangxi Science and Technology Department) Gui ke AD19245096Science and Technology Department of Guangxi Zhuang Autonomous (Guangxi Science and Technology Department) Guike AD19245096
6 · The paper itself

Abstract

Bone marrow stromal/stem cells (BMSCs) are generally considered as common progenitors for both osteoblasts and adipocytes in the bone marrow, but show preferential differentiation into adipocytes rather than osteoblasts under aging, thus leading to senile osteoporosis. Accumulated evidences indicate that rejuvenation of BMSCs by autophagic enhancement delays bone aging. Here we synthetized and demonstrated a novel autophagy activator, CXM102 that could induce autophagy in aged BMSCs, resulting in rejuvenation and preferential differentiation into osteoblasts of BMSCs. Furthermore, CXM102 significantly stimulated bone anabolism, reduced marrow adipocytes, and delayed bone loss in middle-age male mice. Mechanistically, CXM102 promoted transcription factor EB (TFEB) nuclear translocation and favored osteoblasts formation both in vitro and in vivo. Moreover, CXM102 decreased serum levels of inflammation and reduced organ fibrosis, leading to a prolonger lifespan in male mice. Our results indicated that CXM102 could be used as an autophagy inducer to rejuvenate BMSCs and shed new lights on strategies for senile osteoporosis and healthyspan improvement.

Indexed as

AutophagyBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsMesenchymal Stem CellsOsteoporosisAgingAnimalsCell DifferentiationCellular SenescenceLongevityMaleMiceMice, Inbred C57BLOsteoblastsOsteogenesisRejuvenationBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsTcfeb protein, mouse

Identifiers

PMID39164234
PMCPMC11336217

What Socratic 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 Socratic graph.