ArticlePloS one2017
Impairment of Excitation-Contraction Coupling in Right Ventricular Hypertrophied Muscle with Fibrosis Induced by Pulmonary Artery Banding.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 23 citations in OpenAlex.
- Dual inhibition of TGFβ and PDGF improves RV remodeling and function in response to RV pressure or volume-loading.Physiological reports · 2025Article
- Cardiorenal Syndrome in Right Heart Failure Due to Pulmonary Arterial Hypertension-The Right Ventricle as a Therapeutic Target to Improve Renal Function.Cardiovascular drugs and therapy · 2025Review
- Untangling the mechanisms of pulmonary arterial hypertension-induced right ventricular stiffening in a large animal model.Acta biomaterialia · 2023Article
- Pressure Overload and Right Ventricular Failure: From Pathophysiology to Treatment.Journal of clinical medicine · 2023Review
- Untangling the mechanisms of pulmonary hypertension-induced right ventricular stiffening in a large animal model.bioRxiv : the preprint server for biology · 2023Article
- Reversal of Right Ventricular Hypertrophy and Dysfunction by Prostacyclin in a Rat Model of Severe Pulmonary Arterial Hypertension.International journal of molecular sciences · 2022Article
- Imaging of cardiac fibroblast activation in patients with chronic thromboembolic pulmonary hypertension.European journal of nuclear medicine and molecular imaging · 2022Article
- Cardiac Fibrosis in the Pressure Overloaded Left and Right Ventricle as a Therapeutic Target.Frontiers in cardiovascular medicine · 2022Review
- α7 Nicotinic acetylcholine receptor mediates right ventricular fibrosis and diastolic dysfunction in pulmonary hypertension.JCI insight · 2021Article
- Troponin T amino acid mutation (ΔK210) knock-in mice as a neonatal dilated cardiomyopathy model.Pediatric research · 2021Article
- Importance of Cx43 for Right Ventricular Function.International journal of molecular sciences · 2021Review
- Treatment Targets for Right Ventricular Dysfunction in Pulmonary Arterial Hypertension.JACC. Basic to translational science · 2020Review
- Fibrosis growth factor 23 is a promoting factor for cardiac fibrosis in the presence of transforming growth factor-β1.PloS one · 2020Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interstitial myocardial fibrosis is one of the factors responsible for dysfunction of the heart. However, how interstitial fibrosis affects cardiac function and excitation-contraction coupling (E-C coupling) has not yet been clarified. We developed an animal model of right ventricular (RV) hypertrophy with fibrosis by pulmonary artery (PA) banding in rats. Two, four, and six weeks after the PA-banding operation, the tension and intracellular Ca2+ concentration of RV papillary muscles were simultaneously measured (n = 33). The PA-banding rats were clearly divided into two groups by the presence or absence of apparent interstitial fibrosis in the papillary muscles: F+ or F- group, respectively. The papillary muscle diameter and size of myocytes were almost identical between F+ and F-, although the RV free wall weight was heavier in F+ than in F-. F+ papillary muscles exhibited higher stiffness, lower active tension, and lower Ca2+ responsiveness compared with Sham and F- papillary muscles. In addition, we found that the time to peak Ca2+ had the highest correlation coefficient to percent of fibrosis among other parameters, such as RV weight and active tension of papillary muscles. The phosphorylation level of troponin I in F+ was significantly higher than that in Sham and F-, which supports the idea of lower Ca2+ responsiveness in F+. We also found that connexin 43 in F+ was sparse and disorganized in the intercalated disk area where interstitial fibrosis strongly developed. In the present study, the RV papillary muscles obtained from the PA-banding rats enabled us to directly investigate the relationship between fibrosis and cardiac dysfunction, the impairment of E-C coupling in particular. Our results suggest that interstitial fibrosis worsens cardiac function due to 1) the decrease in Ca2+ responsiveness and 2) the asynchronous activation of each cardiac myocyte in the fibrotic preparation due to sparse cell-to-cell communication.
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