Evidence map›Paper›PMID 38403802›Full record

ArticleBiogerontology2024

The SGLT2 inhibitor empagliflozin inhibits skeletal muscle fibrosis in naturally aging male mice through the AMPKα/MMP9/TGF-β1/Smad pathway.

Qixuan Huang, Jie Chen, Siqi Liao, Jiangchuan Long, Ronghua Fang, Yusen He, Peiyun Chen, Dongfang Liu

Abstract read
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In one paragraph

Article in Biogerontology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
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

12 citing papers in PubMed.

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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.

Qixuan Huang *Department of Endocrinology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
Jie Chen *Department of Endocrinology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
Siqi LiaoDepartment of Gastroenterology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
Jiangchuan LongDepartment of Endocrinology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
Ronghua FangDepartment of Endocrinology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
Yusen HeDepartment of Endocrinology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
Peiyun ChenDepartment of Endocrinology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China.
Dongfang LiuDepartment of Endocrinology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, China. ldf023023@qq.com.

Funding

Chongqing Municipal Bureau of Science and Technology cstc2021ycjh-bgzxm0050Chongqing Municipal Health Commission CQYC2020020331
6 · The paper itself

Abstract

abstactWith advancing age, the incidence of sarcopenia increases, eventually leading to a cascade of adverse events. However, there is currently a lack of effective pharmacological treatment for sarcopenia. Sodium-glucose co-transporter 2 inhibitor (SGLT2i) empagliflozin demonstrates anti-fibrotic capabilities in various organs. This study aims to determine whether empagliflozin can improve skeletal muscle fibrosis induced by sarcopenia in naturally aging mice. A natural aging model was established by feeding male mice from 13 months of age to 19 months of age. A fibrosis model was created by stimulating skeletal muscle fibroblasts with TGF-β1. The Forelimb grip strength test assessed skeletal muscle function, and expression levels of COL1A1, COL3A1, and α-SMA were analyzed by western blot, qPCR, and immunohistochemistry. Additionally, levels of AMPKα/MMP9/TGFβ1/Smad signaling pathways were examined. In naturally aging mice, skeletal muscle function declines, expression of muscle fibrosis markers increases, AMPKα expression is downregulated, and MMP9/TGFβ1/Smad signaling pathways are upregulated. However, treatment with empagliflozin reverses this phenomenon. At the cellular level, empagliflozin exhibits similar anti-fibrotic effects, and these effects are attenuated by Compound C and siAMPKα. Empagliflozin exhibits anti-fibrotic effects, possibly associated with the AMPK/MMP9/TGFβ1/Smad signaling pathways.

Indexed as

AgingAMP-Activated Protein KinasesBenzhydryl CompoundsFibrosisGlucosidesMatrix Metalloproteinase 9Muscle, SkeletalSignal TransductionSmad ProteinsSodium-Glucose Transporter 2 InhibitorsTransforming Growth Factor beta1AnimalsMaleMiceMice, Inbred C57BLSarcopeniaAMP-Activated Protein KinasesBenzhydryl CompoundsempagliflozinGlucosidesMatrix Metalloproteinase 9Mmp9 protein, mouseSmad ProteinsSodium-Glucose Transporter 2 InhibitorsTgfb1 protein, mouseTransforming Growth Factor beta1AMPKαEmpagliflozinFibrosisSarcopeniaSmadTGFβ1

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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.