ArticleActa pharmacologica Sinica2010
Protective action of tetramethylpyrazine phosphate against dilated cardiomyopathy in cTnT(R141W) transgenic mice.
Article in Acta pharmacologica Sinica, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Smooth Muscle Cell-Derived Exosomal miR-30a-5p as a Novel Therapeutic Strategy for Erectile Dysfunction in Diabetes Mellitus.Andrology · 2026Article
- Cas13b-mediated RNA targeted therapy alleviates genetic dilated cardiomyopathy in mice.Cell & bioscience · 2024Article
- Integrated bioinformatics analysis for identifying key genes and pathways in female and male patients with dilated cardiomyopathy.Scientific reports · 2023Article
- Postnatal Growth Restriction in Mice Alters Cardiac Protein Composition and Leads to Functional Impairment in Adulthood.International journal of molecular sciences · 2020Article
- Identification of target genes in cardiomyopathy with fibrosis and cardiac remodeling.Journal of biomedical science · 2018Article
- Synthesis, biological evaluation, and pharmacokinetic study of novel liguzinediol prodrugs.Molecules (Basel, Switzerland) · 2013Article
- Article
- Mechanisms and Clinical Application of Tetramethylpyrazine (an Interesting Natural Compound Isolated from Ligusticum Wallichii): Current Status and Perspective.Oxidative medicine and cellular longevityReview
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimDilated cardiomyopathy (DCM) is the most common cause of heart failure, and pharmacological intervention is not currently available. Here we investigate the effect of tetramethylpyrazine phosphate (TMPP) on the progression of DCM in the cTnT(R141W) transgenic mouse model.
methodsThe cTnT(R141W) transgenic mice aged 2 months were divided into model group and TMPP group, whereas age-matched nontransgenic mice were used as wild-type control. TMPP 45 mg.kg(-1).d(-1) was administered for 7 months. Following assessment of cardiac function by echocardiography, cardiac tissues were prepared for histology and electron microscopy. Levels of molecular markers for cardiomyocyte hypertrophy and fibrosis were detected by RT-PCR. Expression of structural proteins of the sarcomere and intercalated disc was determined by Western blot.
resultsTMPP significantly prevented cardiac dilatation and dysfunction with the development of DCM, and decreased mortality by 54%. TMPP decreased HW/BW ratios and expression of hypertrophic markers BNP and ACTA1, as well as reduced interstitial collagen deposition and expression of profibrotic markers Col1a1 and Col3a1. TMPP attenuated ultrastructural disruption caused by cTnT(R141W) expression and decreased expression of structural proteins myotilin and E-cadherin which were up-regulated in the cTnT(R141W) heart. Moreover, TMPP reduced the mRNA expression of Calm1 and Camk2b in the cTnT(R141W) heart.
conclusionOur results suggest that TMPP could be a promising drug for prevention and treatment of DCM.
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