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Ethnopharmacological Relevance: Ganoderic acid A (GAA, CHO) is one of the most abundant and active components of Ganoderic acids (GAs). GAs are highly oxidized tetracyclic triterpenoid compounds mainly derived from Ganoderma lucidum (Curtis) P. Karst (Chinese: ). GAA is primarily isolated from the fruiting body of Ganoderma lucidum. Modern pharmacological investigations have established the broad pharmacological effects of GAA, highlighting its notable influence on managing various conditions, including inflammatory diseases, neurodegenerative diseases, and cancer. This review provides a comprehensive summary of GAA's pharmacological activities.
Material And Methods: The literature in this review were searched in PubMed and China National Knowledge Infrastructure (CNKI) using the keywords "Ganoderic acid A″, "Pharmacology" and "Pharmacokinetics". The literature cited in this review dates from 2000 to 2024.
Results: According to the data, GAA exerts anti-inflammatory, antioxidant, antitumor, neuropsychopharmacological, hepatoprotective, cardiovascular, renoprotective, and lung protective effects by regulating a variety of signal transduction pathways, such as nuclear factor kappa-B (NF-κB), Janus kinase/signal transducer and activator of transcription (JAK/STAT), Toll-like receptor 4 (TLR4), nuclear factor erythroid 2-related factor-2 (Nrf2), phosphoinositide-3-kinase (PI3K)/AKT, mammalian target of rapamycin (mTOR), mitogen-activated protein kinase (MAPK), and Notch. Given its promising pharmacological activity, GAA holds excellent potential for treating human diseases. The pharmacokinetic properties of GAA have also been reviewed, revealing low bioavailability but high absorption and elimination rates. In addition, network pharmacology and molecular docking analyses verified that GAA plays a role in multiple diseases through MAPK3, tumor necrosis factor (TNF), caspase-3 (CASP3), peroxisome proliferator-activated receptor gamma (PPARG), and β-catenin (CTNNB1) signaling pathways.
Conclusion: GAA plays a pivotal role in various pathological and physiological processes, boasting broad application prospects. Furthermore, the network pharmacological results reveal the mechanisms of GAA in the treatment of multiple diseases. In the future, it is necessary to conduct further experiments to elucidate its specific mechanism of action, thus laying the foundation for the scientific utilization of GAA.
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http://dx.doi.org/10.1016/j.jep.2025.119868 | DOI Listing |
Am J Med Genet A
September 2025
Department of Pediatrics, Taipei Veterans General Hospital, Taipei, Taiwan.
Pompe disease (PD), a severe inherited metabolic myopathy caused by the deficiency of acid α-glucosidase (GAA), is characterized by progressive myopathy with reduced muscle strength, endurance, and respiratory insufficiency. The primary GAA deficiency treatment is enzyme replacement therapy (ERT) with alglucosidase alfa; however, its long-term efficacy seems to diminish with time. In 2021, a new ERT medication, avalglucosidase alfa, was approved for patients over 6 months of age with PD in Taiwan.
View Article and Find Full Text PDFLong COVID affects a substantial proportion of the over 778 million individuals infected with SARS-CoV-2, yet predictive models remain limited in scope. While existing efforts, such as the National COVID Cohort Collaborative (N3C), have leveraged electronic health record (EHR) data for risk prediction, accumulating evidence points to additional contributions from social, behavioral, and genetic factors. Using a diverse cohort of SARS-CoV-2-infected individuals (n>17,200) from the NIH All of Us Research Program, we investigated whether integrating EHR data with survey-based and genomic information improves model performance.
View Article and Find Full Text PDFStem Cell Res
August 2025
Université Paris-Saclay, Université d'Evry, Inserm, IStem, UMR861, Corbeil-Essonnes, France; IStem, CECS, Corbeil-Essonnes, France. Electronic address:
Glycogen storage disease type II (GSDII), or Pompe disease, is a rare autosomal recessive metabolic disorder characterized by the deficiency of the lysosomal enzyme acid alpha-glucosidase (GAA). GAA deficiency results in the progressive accumulation of glycogen in cardiac and skeletal muscle tissues, leading to cellular dysfunction and clinical manifestations, including muscle weakness, respiratory difficulties, and cardiomyopathy. In this study, we report the derivation of three induced pluripotent stem cell (iPSC) lines from peripheral blood mononuclear cells of GSDII patients.
View Article and Find Full Text PDFCerebellum
September 2025
Department of Neurology, The Johns Hopkins School of Medicine, Baltimore, MD, USA.
Spinocerebellar ataxia type 27B (SCA27B), caused by GAA repeat expansions in FGF14, is an increasingly recognized form of late-onset cerebellar ataxia. However, early diagnosis remains challenging due to mild or absent cerebellar motor signs and often normal brain magnetic resonance imaging (MRI). Oculovestibular abnormalities, although prevalent, are frequently overlooked and not captured by standard clinical scales such as the Scale for the Assessment and Rating of Ataxia (SARA).
View Article and Find Full Text PDFmedRxiv
August 2025
Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, MD, USA.
Pathogenic GAA repeat expansions in are an established cause of late-onset cerebellar ataxia, but have not been linked to Parkinson's disease (PD). Given emerging evidence that repeat expansions in ataxia-associated genes like , can contribute to atypical or familial forms of PD, we investigated whether expansions might play a similar role. Using long-read whole-genome sequencing on 411 individuals with PD and 197 neurologically healthy controls from the PPMI cohort, alongside 1,429 additional controls from the NIH CARD initiative, the 1000 Genomes Project, and the All of Us program, representing globally diverse populations.
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