Evidence map›Paper›PMID 38284902›Full record

ArticleAging2024

Sesamin-mediated high expression of

Baining Zhang, Zhiwei He, Jialin Guo, Feng Li, Zhi Huang, Wenkai Zheng, Wenhua Xing, Manglai Li, Yong Zhu, Xuejun Yang

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Aging, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
4.2field-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

6 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
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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 3 institutions in 1 country.

Baining ZhangInner Mongolia Medical University, Hohhot, Inner Mongolia, China.
Zhiwei HeInner Mongolia Medical University, Hohhot, Inner Mongolia, China.
Jialin GuoInner Mongolia Medical University, Hohhot, Inner Mongolia, China.
Feng LiDepartment of Spine Surgery, Area A, The Second Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia, China.
Zhi HuangDepartment of Spine Surgery, Area A, The Second Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia, China.
Wenkai ZhengDepartment of Spine Surgery, Area A, The Second Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia, China.
Wenhua XingDepartment of Spine Surgery, Area A, The Second Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia, China.
Manglai LiDepartment of Bone and Soft Tissue Oncology, The Affiliated People’s Hospital of inner Mongolia Medical University, Peking University Cancer Hospital, Hohhot, Inner Mongolia, China.
Yong ZhuDepartment of Bone and Soft Tissue Oncology, The Affiliated People’s Hospital of inner Mongolia Medical University, Peking University Cancer Hospital, Hohhot, Inner Mongolia, China.
Xuejun YangDepartment of Spine Surgery, Area A, The Second Affiliated Hospital of Inner Mongolia Medical University, Hohhot, Inner Mongolia, China.
Second Affiliated Hospital of Inner Mongolia Medical University · CNInner Mongolia Medical University · CNPeking University Cancer Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lumbar disc degeneration (LDD) is a prevalent clinical spinal disease characterized by the calcification and degeneration of the cartilage endplate (CEP), which significantly reduces nutrient supply to the intervertebral disc. Traditional Chinese medicine offers a conservative and effective approach for treating LDD. We aimed to investigate the molecular mechanisms underlying the therapeutic effects of Sesamin in LDD treatment. Transcriptome sequencing was used to analyze the effect of Sesamin on LPS-induced ATDC5. We explored the role of BECN2, a target gene of Sesamin, in attenuating LPS-induced degeneration of ATDC5 cells. Our results revealed the identification of 117 differentially expressed genes (DEGs), with 54 up-regulated and 63 down-regulated genes. Notably, Sesamin significantly increased the expression of BECN2 in LPS-induced ATDC5 cell degeneration. Overexpressed BECN2 enhanced cell viability and inhibited cell apoptosis in LPS-induced ATDC5 cells, while BECN2 knockdown reduced cell viability and increased apoptosis. Furthermore, BECN2 played a crucial role in attenuating chondrocyte degeneration by modulating autophagy and inflammation. Specifically, BECN2 suppressed autophagy by reducing the expression of ATG14, VPS34, and GASP1, and alleviated the inflammatory response by decreasing the expression of inflammasome proteins NLRP3, NLRC4, NLRP1, and AIM2.

Indexed as

DioxolesIntervertebral Disc DegenerationIntracellular Signaling Peptides and ProteinsLignansAnimalsAutophagyCartilageInflammationLipopolysaccharidesMiceBecn2 protein, mouseDioxolesIntracellular Signaling Peptides and ProteinsLignansLipopolysaccharidessesaminautophagyBECN2cartilage endplate degenerationinflammationSesamin

Identifiers

PMID38284902
PMCPMC10866406
OpenAlexW4391263224

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.