Evidence map›Paper›PMID 33405354›Full record

ArticleJournal of cellular and molecular medicine2021

Formononetin ameliorates muscle atrophy by regulating myostatin-mediated PI3K/Akt/FoxO3a pathway and satellite cell function in chronic kidney disease.

Lingyu Liu, Rong Hu, Haiyan You, Jingjing Li, Yangyang Liu, Qiang Li, Xiaohui Wu, Jiawen Huang, Xiangsheng Cai, Mingqing Wang and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
3.3field-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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 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

11 authors at 4 institutions in 1 country.

Lingyu LiuShenzhen Hospital, Southern Medical University, Shenzhen, China.
Rong HuSchool of Traditional Chinese Medicine, Southern Medical University, Guangzhou, China.
Haiyan YouShenzhen Hospital, Southern Medical University, Shenzhen, China.
Jingjing LiInstitute of Biotherapy, Southern Medical University, Guangzhou, China.
Yangyang LiuHuangpu People's Hospital of Zhongshan, Zhongshan, China.
Qiang LiShenzhen Hospital, Southern Medical University, Shenzhen, China.
Xiaohui WuShenzhen Hospital, Southern Medical University, Shenzhen, China.
Jiawen HuangShenzhen Hospital, Southern Medical University, Shenzhen, China.
Xiangsheng CaiCenter for Medical Experiments, University of Chinese Academy of Science-Shenzhen Hospital, Shenzhen, China.
Mingqing WangSchool of Traditional Chinese Medicine, Southern Medical University, Guangzhou, China.
Lianbo WeiShenzhen Hospital, Southern Medical University, Shenzhen, China.ORCID 0000-0001-6657-0290
Southern Medical University Shenzhen Hospital · CNSouthern Medical University · CNShenzhen Institutes of Advanced Technology · CNZhongshan People's Hospital · CN

Funding

National Natural Science Foundation of China 81774035National Natural Science Foundation of China 81774094
6 · The paper itself

Abstract

Muscle atrophy is a common complication in chronic kidney disease (CKD). Inflammation and myostatin play important roles in CKD muscle atrophy. Formononetin (FMN), which is a major bioactive isoflavone compound in Astragalus membranaceus, exerts anti-inflammatory effects and the promotion of myogenic differentiation. Our study is based on myostatin to explore the effects and mechanisms of FMN in relation to CKD muscle atrophy. In this study, CKD rats and tumour necrosis factor α (TNF-α)-induced C2C12 myotubes were used for in vivo and in vitro models of muscle atrophy. The results showed that FMN significantly improved the renal function, nutritional status and inflammatory markers in CKD rats. Values for bodyweight, weight of tibialis anterior and gastrocnemius muscles, and cross-sectional area (CSA) of skeletal muscles were significantly larger in the FMN treatment rats. Furthermore, FMN significantly suppressed the expressions of MuRF-1, MAFbx and myostatin in the muscles of CKD rats and the TNF-α-induced C2C12 myotubes. Importantly, FMN significantly increased the phosphorylation of PI3K, Akt, and FoxO3a and the expressions of the myogenic proliferation and differentiation markers, myogenic differentiation factor D (MyoD) and myogenin in muscles of CKD rats and the C2C12 myotubes. Similar results were observed in TNF-α-induced C2C12 myotubes transfected with myostatin-small interfering RNA (si-myostatin). Notably, myostatin overexpression plasmid (myostatin OE) abolished the effect of FMN on the phosphorylation of the PI3K/Akt/FoxO3a pathway and the expressions of MyoD and myogenin. Our findings suggest that FMN ameliorates muscle atrophy related to myostatin-mediated PI3K/Akt/FoxO3a pathway and satellite cell function.

Indexed as

AnimalsCell DifferentiationCell ProliferationDisease Models, AnimalDisease SusceptibilityForkhead Box Protein O3IsoflavonesMaleMiceMuscular AtrophyMyostatinPhosphatidylinositol 3-KinasesPhosphorylationProto-Oncogene Proteins c-aktRatsRenal Insufficiency, ChronicForkhead Box Protein O3formononetinFOXO3 protein, ratIsoflavonesMyostatinPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktformononetininflammationmuscle atrophymyostatinPI3K/Akt/FoxO3asatellite cell function

Identifiers

PMID33405354
PMCPMC7875933
OpenAlexW3118670077

What OpenQuestion 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 OpenQuestion graph.