ArticleJournal of the American College of Cardiology2006
Antifibrotic effects of antioxidant N-acetylcysteine in a mouse model of human hypertrophic cardiomyopathy mutation.
Article in Journal of the American College of Cardiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 123 citations in OpenAlex.
- Hypertrophy Regression With N-Acetylcysteine in Hypertrophic Cardiomyopathy (HALT-HCM): A Randomized, Placebo-Controlled, Double-Blind Pilot Study.Circulation research · 2018Trial
- SGLT2 Inhibitors in Hypertrophic Cardiomyopathy: Emerging Evidence and Putative Mechanisms.Biomolecules · 2026Review
- Mechano-energetic uncoupling in heart failure.Nature reviews. Cardiology · 2025Review
- Therapy to teratology: chronic paternal antioxidant supplementation alters offspring placental architecture and craniofacial morphogenesis in a mouse model.Frontiers in cell and developmental biology · 2025Article
- Influencing and prognostic factors of end-stage hypertrophic cardiomyopathy.ESC heart failure · 2024Article
- Hypertrophic cardiomyopathy-associated mutations drive stromal activation via EGFR-mediated paracrine signaling.Science advances · 2024Article
- Necroptosis and immune infiltration in hypertrophic cardiomyopathy: novel insights from bioinformatics analyses.Frontiers in cardiovascular medicine · 2024Article
- Down-regulation of the Smad signaling by circZBTB46 via the Smad2-PDLIM5 axis to inhibit type I collagen expression.Journal of geriatric cardiology : JGC · 2023Article
- Mechano-energetic uncoupling in hypertrophic cardiomyopathy: Pathophysiological mechanisms and therapeutic opportunities.Journal of molecular and cellular cardiology plus · 2023Review
- Circulating MicroRNAs Identify Early Phenotypic Changes in Sarcomeric Hypertrophic Cardiomyopathy.Circulation. Heart failure · 2023Article
- Targeting lipid metabolism as a new therapeutic strategy for inherited cardiomyopathies.Frontiers in cardiovascular medicine · 2023Review
- What Causes Hypertrophic Cardiomyopathy?The American journal of cardiology · 2022Review
- Review
- Metabolic characterization of hypertrophic cardiomyopathy in human heart.Nature cardiovascular research · 2022Article
- Atypical antipsychotics and oxidative cardiotoxicity: review of literature and future perspectives to prevent sudden cardiac death.Journal of geriatric cardiology : JGC · 2021Article
- Pushing the Limits of Medical Management in HCM: A Review of Current Pharmacological Therapy Options.International journal of molecular sciences · 2021Review
- Molecular Genetic Basis of Hypertrophic Cardiomyopathy.Circulation research · 2021Article
- Article
- Predictive values of multiple non-invasive markers for myocardial fibrosis in hypertrophic cardiomyopathy patients with preserved ejection fraction.Scientific reports · 2021Article
- Individualized interactomes for network-based precision medicine in hypertrophic cardiomyopathy with implications for other clinical pathophenotypes.Nature communications · 2021Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
objectivesThe objective was to determine the effects of antioxidant N-acetylcysteine (NAC) on reversal and attenuation of established interstitial fibrosis in the cardiac troponin T (cTnT) mouse model of human hypertrophic cardiomyopathy (HCM) mutation.
backgroundInterstitial fibrosis is a characteristic pathological feature of HCM and a risk factor for sudden cardiac death. The cTnT-Q92 transgenic mice, generated by cardiac-restricted expression of human HCM mutation, show a two- to four-fold increase in interstitial fibrosis.
methodsWe randomized the cTnT-Q92 mice to treatment with a placebo or NAC (250, 500, or 1,000 mg/kg/day) and included non-transgenic mice as controls (N = 5 to 13 per group). We performed echocardiography before and 24 weeks after therapy, followed by histologic and molecular characterization.
resultsThere were no significant differences in the baseline characteristics of the groups. Treatment with NAC reduced myocardial concentrations of malondialdehyde and 4-hydroxy-2(E)-nonenal, markers of oxidative stress, by 40%. Collagen volume fractions comprised 1.94 +/- 0.76% of the myocardium in non-transgenic, 6.2 +/- 1.65% in the placebo, and 1.56 +/- 0.98% in the NAC (1,000 mg/kg/day) groups (p < 0.001). Expression levels of Col1a1 and Col1a2 were also reduced significantly, as were levels of phosphorylated but not total p44/42, p38, and c-Jun NH2-terminal kinase. Levels of oxidized mitochondrial and nuclear DNA were not significantly different.
conclusionsTreatment with NAC reduced myocardial oxidative stress, stress-responsive signaling kinases, and fibrosis in a mouse model of HCM. The potential beneficial effects of NAC in reversal of cardiac phenotype in human HCM, the most common cause of sudden cardiac death in the young, merits investigation.
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