Evidence map›Paper›PMID 42848624›Full record

ArticleArquivos brasileiros de cardiologia2026

Astragalus Polysaccharide Enhances Mitochondrial Biogenesis and Function in Cardiomyocytes Through AMPK Activation.

Chengbin Wang, Shuhan Lv, Xingde Liu

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Article in Arquivos brasileiros de cardiologia, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

3 authors.

Chengbin WangGuizhou University of Traditional Chinese Medicine - Department of Second Clinical Medical College, Guiyang - China.ORCID http://orcid.org/0009-0009-8475-9447
Shuhan LvGuizhou University of Traditional Chinese Medicine - Department of Second Clinical Medical College, Guiyang - China.ORCID http://orcid.org/0009-0000-7772-5200
Xingde LiuGuizhou University of Traditional Chinese Medicine - Department of Second Clinical Medical College, Guiyang - China.ORCID http://orcid.org/0009-0002-5613-7033

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMitochondrial dysfunction is a key driver of heart failure, underscoring the need for therapies that promote mitochondrial biogenesis and function. Astragalus polysaccharide (APS), a bioactive compound from Astragalus membranaceus, has demonstrated cardioprotective properties, but its direct effects on mitochondrial homeostasis in cardiomyocytes remain unclear.

objectivesThis study aimed to investigate the effects of APS on mitochondrial function and biogenesis in HL-1 cardiomyocytes and to elucidate the involvement of the AMP-activated protein kinase (AMPK)/peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) signaling pathway.

methodsHL-1 cardiomyocytes were treated with non-toxic concentrations of APS (1.25-2.5 g/L) for 48 hours. Mitochondrial respiration was assessed via Seahorse XF Analyzer, adenosine triphosphate (ATP) levels were quantified, and Complex IV activity was measured. Mitochondrial biogenesis was evaluated by mitochondrial DNA (mtDNA)/ nuclear DNA (nDNA) ratio, cytochrome B levels, and mitochondrial mass. Key proteins and genes, including PGC-1α, nuclear respiratory factor 2 (NRF2), mitochondrial transcription factor A (TFAM), uncoupling protein 2 (UCP2), and phosphorylated AMPK (p-AMPK), were analyzed by Western blot and qPCR. The AMPK inhibitor Compound C was used to confirm the pathway's role.

resultsAPS treatment significantly enhanced mitochondrial respiration, ATP production, and Complex IV activity. It promoted mitochondrial biogenesis, evidenced by increased mtDNA/nDNA ratio and mitochondrial mass. APS upregulated the expression of PGC-1α, NRF2, TFAM, and UCP2, and activated AMPK phosphorylation. All these beneficial effects were abolished by AMPK inhibition with Compound C.

conclusionsAPS enhances mitochondrial biogenesis and function in cardiomyocytes through activation of the AMPK/PGC-1α signaling pathway, identifying it as a potential therapeutic agent for cardiac diseases associated with mitochondrial dysfunction.

Indexed as

AMP-Activated Protein KinasesAstragalus PlantMitochondria, HeartMitochondrial TurnoverMyocytes, CardiacOrganelle BiogenesisPolysaccharidesAdenosine TriphosphateAnimalsDNA, MitochondrialMicePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaSignal TransductionTime FactorsTranscription FactorsAdenosine TriphosphateAMP-Activated Protein KinasesDNA, MitochondrialPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPolysaccharidesTranscription Factors

Identifiers

PMID42848624
PMCPMC13671154

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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.