Evidence map›Paper›PMID 37163424›Full record

ArticleAging and disease2023

C-Phycocyanin Ameliorates the Senescence of Mesenchymal Stem Cells through ZDHHC5-Mediated Autophagy via PI3K/AKT/mTOR Pathway.

Guoxiang Liu, Xiaoxia Li, Fanghao Yang, Jingyu Qi, Lipeng Shang, Huhu Zhang, Shuang Li, Fenghua Xu, Lingne Li, Huaxin Yu and 13 more

Open access · goldAbstract read
In one paragraph

Article in Aging and disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 11% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 11 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

23 authors at 4 institutions in 1 country.

Guoxiang LiuDepartment of Genetics and Cell Biology, Basic Medical College, Qingdao University, Qingdao, China.
Xiaoxia LiDepartment of Genetics and Cell Biology, Basic Medical College, Qingdao University, Qingdao, China.
Fanghao YangDepartment of Genetics and Cell Biology, Basic Medical College, Qingdao University, Qingdao, China.
Jingyu QiDepartment of Genetics and Cell Biology, Basic Medical College, Qingdao University, Qingdao, China.
Lipeng ShangDepartment of Genetics and Cell Biology, Basic Medical College, Qingdao University, Qingdao, China.
Huhu ZhangDepartment of Genetics and Cell Biology, Basic Medical College, Qingdao University, Qingdao, China.
Shuang LiDepartment of Genetics and Cell Biology, Basic Medical College, Qingdao University, Qingdao, China.
Fenghua XuDepartment of Genetics and Cell Biology, Basic Medical College, Qingdao University, Qingdao, China.
Lingne LiDepartment of Genetics and Cell Biology, Basic Medical College, Qingdao University, Qingdao, China.
Huaxin YuDepartment of Genetics and Cell Biology, Basic Medical College, Qingdao University, Qingdao, China.
Yang LiDepartment of Genetics and Cell Biology, Basic Medical College, Qingdao University, Qingdao, China.
Xiaolei DongDepartment of Genetics and Cell Biology, Basic Medical College, Qingdao University, Qingdao, China.
Qinghang SongDepartment of Genetics and Cell Biology, Basic Medical College, Qingdao University, Qingdao, China.
Feng ZhuDepartment of Genetics and Cell Biology, Basic Medical College, Qingdao University, Qingdao, China.
Guang ChenDepartment of Genetics and Cell Biology, Basic Medical College, Qingdao University, Qingdao, China.
Can CaoDepartment of Genetics and Cell Biology, Basic Medical College, Qingdao University, Qingdao, China.
Liangqian JiangDepartment of Medical Genetics, Linyi People's Hospital, Linyi, China.
Junzhe SuDepartment of Genetics and Cell Biology, Basic Medical College, Qingdao University, Qingdao, China.
Lina YangDepartment of Genetics and Cell Biology, Basic Medical College, Qingdao University, Qingdao, China.
Xiaohui XuDepartment of Genetics and Cell Biology, Basic Medical College, Qingdao University, Qingdao, China.
Zhe ZhangDepartment of Genetics and Cell Biology, Basic Medical College, Qingdao University, Qingdao, China.
Robert Chunhua ZhaoCollege of Basic Medicine, Institute of Stem Cell and Regenerative Medicine, Qingdao University, Qingdao, China.
Bing LiDepartment of Genetics and Cell Biology, Basic Medical College, Qingdao University, Qingdao, China.
Qingdao University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNLinyi People's Hospital · CNShanghai University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The senescence of mesenchymal stem cells (MSCs) impairs their regenerative capacity to maintain tissue homeostasis. Numerous studies are focusing on the interventions and mechanisms to attenuate the senescence of MSCs. C-phycocyanin (C-PC) is reported to have multiple functions such as antitumor, antioxidation, anti-inflammation and anti-aging roles, but there is little research about the effects of C-PC on the senescence of MSCs. Here we investigated the roles and mechanism of C-PC on MSCs senescence. In vitro results showed that C-PC could reduce senescence, enhance proliferation, promote the adipogenic and osteogenic differentiation in senescent MSCs induced by oxidative stress. In vivo D-Galactose (D-Gal) induced rats aging models showed C-PC also increased the viability and differentiation of intrinsic senescent bone marrow derived MSCs (BMSCs). Furthermore, C-PC also decreased the levels of oxidative stress markers ROS or MDA, elevated the SOD activity, and increased the anti-inflammatory factors. Proteomic chip analysis showed that C-PC interacted with ZDHHC5, and their interaction was verified by pull down assay. Overexpression of ZDHHC5 aggravated the senescence of MSCs and greatly lessened the beneficial effects of C-PC on senescence. In addition, we found ZDHHC5 regulated autophagy by altering LC3, Beclin1 and PI3K/AKT/mTOR pathway. In summary, our data indicated that C-PC ameliorates the senescence of MSCs through zinc finger Asp-His-His-Cys (DHHC) domain-containing protein 5 (ZDHHC5) mediated autophagy via PI3K/AKT/mTOR pathway. The present study uncovered the key role of autophagy in MSCs senescence and PI3K/AKT/mTOR pathway may be a potential target for anti-senescence studies of MSCs.

Identifiers

PMID37163424
PMCPMC10389819
OpenAlexW4360595268

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.