Evidence map›Paper›PMID 35370668›Full record

ArticleFrontiers in pharmacology2022

Paeoniflorin Ameliorates Skeletal Muscle Atrophy in Chronic Kidney Disease

Qiang Li, Jing Wu, Jiawen Huang, Rong Hu, Haiyan You, Lingyu Liu, Dongtao Wang, Lianbo Wei

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 8% 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

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

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  20. Mitochondria-Nuclear Crosstalk: Orchestrating mtDNA Maintenance.Environmental and molecular mutagenesis · 2025
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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 at 4 institutions in 1 country.

Qiang LiDepartment of Traditional Chinese Medicine, Shenzhen Hospital, Southern Medical University, Shenzhen, China.
Jing WuDepartment of Rheumatology and Clinical Immunology, Zhujiang Hospital, Southern Medical University, Guangzhou, China.
Jiawen HuangDepartment of Traditional Chinese Medicine, Shenzhen Hospital, Southern Medical University, Shenzhen, China.
Rong HuSchool of Traditional Chinese Medicine, Southern Medical University, Guangzhou, China.
Haiyan YouSchool of Traditional Chinese Medicine, Southern Medical University, Guangzhou, China.
Lingyu LiuFirst Affiliated Hospital of Henan University of Chinese Medicine, Zhengzhou, China.
Dongtao WangDepartment of Traditional Chinese Medicine, Shenzhen Hospital, Southern Medical University, Shenzhen, China.
Lianbo WeiDepartment of Traditional Chinese Medicine, Shenzhen Hospital, Southern Medical University, Shenzhen, China.
Southern Medical University · CNSouthern Medical University Shenzhen Hospital · CNFirst Affiliated Hospital of Henan University · CNZhujiang Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Skeletal muscle atrophy is a common and serious complication of chronic kidney disease (CKD). Oxidative stress and mitochondrial dysfunction are involved in the pathogenesis of muscle atrophy. The aim of this study was to explore the effects and mechanisms of paeoniflorin on CKD skeletal muscle atrophy. We demonstrated that paeoniflorin significantly improved renal function, calcium/phosphorus disorders, nutrition index and skeletal muscle atrophy in the 5/6 nephrectomized model rats. Paeoniflorin ameliorated the expression of proteins associated with muscle atrophy and muscle differentiation, including muscle atrophy F-box (MAFbx/atrogin-1), muscle RING finger 1 (MuRF1), MyoD and myogenin (MyoG). In addition, paeoniflorin modulated redox homeostasis by increasing antioxidant activity and suppressing excessive accumulation of reactive oxygen species (ROS). Paeoniflorin alleviated mitochondrial dysfunction by increasing the activities of electron transport chain complexes and mitochondrial membrane potential. Furthermore, paeoniflorin also regulates mitochondrial dynamics. Importantly, paeoniflorin upregulated the expression of silent information regulator 1 (SIRT1), peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α), and phosphorylation of AMP-activated protein kinase (AMPK). Similar results were observed in C2C12 myoblasts treated with TNF-α and paeoniflorin. Notably, these beneficial effects of paeoniflorin on muscle atrophy were abolished by inhibiting AMPK and SIRT1 and knocking down PGC-1α. Taken together, this study showed for the first time that paeoniflorin has great therapeutic potential for CKD skeletal muscle atrophy through AMPK/SIRT1/PGC-1α-mediated oxidative stress and mitochondrial dysfunction.

Indexed as

AMPK/SIRT1/PGC-1αchronic kidney diseasemitochondrial dysfunctionoxidative stresspaeoniflorinskeletal muscle atrophy

Identifiers

PMID35370668
PMCPMC8964350
OpenAlexW4220658914

What OpenQuestion 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 OpenQuestion graph.