ArticleAmerican journal of physiology. Lung cellular and molecular physiology2017
Effect of α7 nicotinic acetylcholine receptor activation on cardiac fibroblasts: a mechanism underlying RV fibrosis associated with cigarette smoke exposure.
Article in American journal of physiology. Lung cellular and molecular physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.
- Guidelines for measuring cardiac physiology in mice.American journal of physiology. Heart and circulatory physiology · 2018Guideline
- CDX1 improves nicotine induced cardiac fibroblasts activation and cardiomyocyte hypertrophy by alleviating autophagic flux impairment through modulation of LAPTM4B.Scientific reports · 2025Article
- Endothelial Cpt1a Inhibits Neonatal Hyperoxia-Induced Pulmonary Vascular Remodeling by Repressing Endothelial-Mesenchymal Transition.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Assessment of the alpha 7 nicotinic acetylcholine receptor as an imaging marker of cardiac repair-associated processes using NS14490.EJNMMI research · 2024Article
- An integral perspective of canonical cigarette and e-cigarette-related cardiovascular toxicity based on the adverse outcome pathway framework.Journal of advanced research · 2023Review
- Nicotine and novel tobacco products drive adverse cardiac remodeling and dysfunction in preclinical studies.Frontiers in cardiovascular medicine · 2022Article
- Article
- Cardioprotective effects of early intervention with sacubitril/valsartan on pressure overloaded rat hearts.Scientific reports · 2021Article
- α7 Nicotinic acetylcholine receptor mediates right ventricular fibrosis and diastolic dysfunction in pulmonary hypertension.JCI insight · 2021Article
- Angiotensin II type 1 receptor mediates pulmonary hypertension and right ventricular remodeling induced by inhaled nicotine.American journal of physiology. Heart and circulatory physiology · 2021Article
- Nicotine and vascular dysfunction.Acta physiologica (Oxford, England) · 2021Review
- Nicotine, smoking, podocytes, and diabetic nephropathy.American journal of physiology. Renal physiology · 2021Article
- Activation of the cardiac non-neuronal cholinergic system prevents the development of diabetes-associated cardiovascular complications.Cardiovascular diabetology · 2021Article
- Donepezil Ameliorates Pulmonary Arterial Hypertension by Inhibiting M2-Macrophage Activation.Frontiers in cardiovascular medicine · 2021Article
- Past as Prologue: Vaping Effects on the Developing Lung.American journal of respiratory cell and molecular biology · 2020Article
- Endothelial to mesenchymal transition during neonatal hyperoxia-induced pulmonary hypertension.The Journal of pathology · 2020Article
- Adaptive and innate immune mechanisms in cardiac fibrosis complicating pulmonary arterial hypertension.Physiological reports · 2020Review
- Article
- Treatment of Pulmonary Hypertension With Angiotensin II Receptor Blocker and Neprilysin Inhibitor Sacubitril/Valsartan.Circulation. Heart failure · 2019Article
- MicroRNA-1-Mediated Inhibition of Cardiac Fibroblast Proliferation Through Targeting Cyclin D2 and CDK6.Frontiers in cardiovascular medicine · 2019Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
Abstract
Right ventricular (RV) dysfunction is associated with numerous smoking-related illnesses, including chronic obstructive pulmonary disease (COPD), in which it is present even in the absence of pulmonary hypertension. It is unknown whether exposure to cigarette smoke (CS) has direct effects on RV function and cardiac fibroblast (CF) proliferation or collagen synthesis. In this study, we evaluated cardiac function and fibrosis in mice exposed to CS and determined mechanisms of smoke-induced changes in CF signaling and fibrosis. AKR mice were exposed to CS for 6 wk followed by echocardiography and evaluation of cardiac hypertrophy, collagen content, and pulmonary muscularization. Proliferation and collagen content were evaluated in primary isolated rat CFs exposed to CS extract (CSE) or nicotine. Markers of cell proliferation, fibrosis, and proliferative signaling were determined by immunoblot or Sircol collagen assay. Mice exposed to CS had significantly decreased RV function, as determined by tricuspid annular plane systolic excursion. There were no changes in left ventricular parameters. RV collagen content was significantly elevated, but there was no change in RV hypertrophy or pulmonary vascular muscularization. CSE directly increased CF proliferation and collagen content in CF. Nicotine alone reproduced these effects. CSE and nicotine-induced fibroblast proliferation and collagen content were mediated through α7 nicotinic acetylcholine receptors and were dependent on PKC-α, PKC-δ, and reduced p38-MAPK phosphorylation. CS and nicotine have direct effects on CFs to induce proliferation and fibrosis, which may negatively affect right heart function.
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Registered trials
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