Evidence map›Paper›PMID 38561613›Full record

ArticleCurrent pharmaceutical design2024

Molecular Mechanisms of Medicinal Plant

Yinhong Zhang, Jing He, Lifeng Xiang, Xinhua Tang, Shiyu Wang, Aoyu Li, Chaoyan Wang, Li Li, Baosheng Zhu

Abstract read
PubMed Publisher
In one paragraph

Article in Current pharmaceutical design, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. Review
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

9 authors at 1 institution in 1 country.

Yinhong ZhangNHC Key Laboratory of Preconception Health Birth in Western China, Yunnan Provincial Key Laboratory for Birth Defects and Genetic Diseases, Department of Medical Genetics, Yunnan Provincial Clinical Research Center for Birth Defects and Rare Diseases, The First People's Hospital of Yunnan Province, Kunming 650032, Yunnan, China.
Jing HeNHC Key Laboratory of Preconception Health Birth in Western China, Yunnan Provincial Key Laboratory for Birth Defects and Genetic Diseases, Department of Medical Genetics, Yunnan Provincial Clinical Research Center for Birth Defects and Rare Diseases, The First People's Hospital of Yunnan Province, Kunming 650032, Yunnan, China.
Lifeng XiangThe First People's Hospital of Yunnan Province, Affiliated Hospital of Kunming University of Science and Technology, Kunming 650032, Yunnan, China.
Xinhua TangNHC Key Laboratory of Preconception Health Birth in Western China, Yunnan Provincial Key Laboratory for Birth Defects and Genetic Diseases, Department of Medical Genetics, Yunnan Provincial Clinical Research Center for Birth Defects and Rare Diseases, The First People's Hospital of Yunnan Province, Kunming 650032, Yunnan, China.
Shiyu WangSchool of Medical, Kunming University of Science and Technology, Kunming 650500, Yunnan, China.
Aoyu LiSchool of Medical, Kunming University of Science and Technology, Kunming 650500, Yunnan, China.
Chaoyan WangSchool of Medical, Kunming University of Science and Technology, Kunming 650500, Yunnan, China.
Li LiThe First People's Hospital of Yunnan Province, Affiliated Hospital of Kunming University of Science and Technology, Kunming 650032, Yunnan, China.
Baosheng ZhuNHC Key Laboratory of Preconception Health Birth in Western China, Yunnan Provincial Key Laboratory for Birth Defects and Genetic Diseases, Department of Medical Genetics, Yunnan Provincial Clinical Research Center for Birth Defects and Rare Diseases, The First People's Hospital of Yunnan Province, Kunming 650032, Yunnan, China.
Kunming University of Science and Technology · CN

Funding

Co-operation Fund of Kunming Medical University and the Science and Technology Department of Yunnan Province 202101AY070001-262"Famous Doctor" special project of the Ten Thousand People Program of Yunnan Province YNWR-MY-2018-016Fund of Yunnan Provincial Clinical Research Center for Birth Defects and Rare Diseases 2019ZF015Innovation Research Project of Human Assisted Reproductive Technology of Yunnan Province 2017HC009Kunming University of Science and Technology & the First People's Hospital of Yunnan Province KUST-KH2022003ZNational Key Research and Development Program of China 2021YFA0805703Open Fund of Reproductive Obstetrics and Gynecology Clinical Center of Yunnan Province zx2019-01-01, 2022LCZXKF-SZ02Open Fund of Yunnan Provincial Key Laboratory for Birth Defects and Genetic Diseases 2020ZDKFKT001Yunnan Provincial Young and Middle-aged Academic and Technical Leaders Reserve Talents Program 202305AC160022
6 · The paper itself

Abstract

backgroundSpinal Muscular Atrophy (SMA) is a severe motor neuronal disorder with high morbidity and mortality. Securinine has shown the potential to treat SMA; however, its anti-SMA role remains unclear.

objectiveThis study aims to reveal the anti-SMA mechanisms of securinine.

methodsSecurinine-associated targets were acquired from Herbal Ingredients' Targets (HIT), Similarity Ensemble Approach (SEA), and SuperPred. SMA-associated targets were obtained from GeneCards and Dis- GeNET. Protein-protein Interaction (PPI) network was constructed using GeneMANIA, and hug targets were screened using cytoHubba. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed using ClusterProfifiler. Molecular docking was conducted using Pymol and Auto- Dock. In vitro assays were used to verify the anti-SMA effects of securinine.

resultsTwenty-six intersection targets of securinine and SMA were obtained. HDAC1, HDAC2, TOP2A, PIK3R1, PRMT5, JAK2, HSP90AB1, TERT, PTGS2, and PAX8 were the core targets in PPI network. GO analysis demonstrated that the intersecting targets were implicated in the regulation of proteins, steroid hormones, histone deacetylases, and DNA transcription. KEGG analysis, pathway-pathway, and hub target-pathway networks revealed that securinine might treat SMA through TNF, JAK-STAT, Ras, and PI3K-Akt pathways. Securinine had a favorable binding affinity with HDAC1, HSP90AB, JAK2, PRMT5, PTGS2, and TERT. Securinine rescued viability suppression, mitochondria damage, and SMN loss in the SMA cell model. Furthermore, securinine increased HDAC1 and PRMT5 expression, decreased PTGS2 expression, suppressed the JAK2-STAT3 pathway, and promoted the PI3K-Akt pathway.

conclusionSecurinine might alleviate SMA by elevating HDAC1 and PRMT5 expression and reducing PTGS2 via JAK2-STAT3 suppression and PI3K-Akt activation.

Indexed as

Muscular Atrophy, SpinalNetwork PharmacologyPlants, MedicinalAzepinesHeterocyclic Compounds, Bridged-RingHumansLactonesMolecular Docking SimulationMolecular StructurePiperidinesAzepinesHeterocyclic Compounds, Bridged-RingLactonesPiperidinessecurinineExperimental verificationgene regulation.network pharmacologysecurininespinal muscular atrophysurvival motor neuron

Identifiers

PMID38561613
OpenAlexW4393444628

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.