‘Targeting the cardiac myocyte and fibrosis’ in heart failure

Ishiura, Junko; Nakamori, Shiro; Ishida, Masaki; Dohi, Kaoru

doi:10.1093/eurheartj/ehab780

Cited by 3 publications

(1 citation statement)

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“…Fibrosis, as a defensive response to acute cardiac injury, contributes to stabilizing the heart and maintaining integrity and normal function to a certain extent [ 33 ]. However, excessive fibrosis reduces cardiac compliance and accelerates the progression of heart failure [ 34 – 36 ]. Our results observed that there was no obvious fibrosis after 1 week and 4 weeks of exposure.…”

Section: Discussionmentioning

confidence: 99%

Multi-dimensional evaluation of cardiotoxicity in mice following respiratory exposure to polystyrene nanoplastics

Zhang,

Yang,

et al. 2023

Part Fibre Toxicol

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Background Nanoplastics (NPs) could be released into environment through the degradation of plastic products, and their content in the air cannot be ignored. To date, no studies have focused on the cardiac injury effects and underlying mechanisms induced by respiratory exposure to NPs. Results Here, we systematically investigated the cardiotoxicity of 40 nm polystyrene nanoplastics (PS-NPs) in mice exposed via inhalation. Four exposure concentrations (0 µg/day, 16 µg/day, 40 µg/day and 100 µg/day) and three exposure durations (1 week, 4 weeks, 12 weeks) were set for more comprehensive information and RNA-seq was performed to reveal the potential mechanisms of cardiotoxicity after acute, subacute and subchronic exposure. PS-NPs induced cardiac injury in a dose-dependent and time-dependent manner. Acute, subacute and subchronic exposure increased the levels of injury biomarkers and inflammation and disturbed the equilibrium between oxidase and antioxidase activity. Subacute and subchronic exposure dampened the cardiac systolic function and contributed to structural and ultrastructural damage in heart. Mechanistically, violent inflammatory and immune responses were evoked after acute exposure. Moreover, disturbed energy metabolism, especially the TCA cycle, in the myocardium caused by mitochondria damage may be the latent mechanism of PS-NPs-induced cardiac injury after subacute and subchronic exposure. Conclusion The present study evaluated the cardiotoxicity induced by respiratory exposure to PS-NPs from multiple dimensions, including the accumulation of PS-NPs, cardiac functional assessment, histology observation, biomarkers detection and transcriptomic study. PS-NPs resulted in cardiac injury structurally and functionally in a dose-dependent and time-dependent manner, and mitochondria damage of myocardium induced by PS-NPs may be the potential mechanism for its cardiotoxicity. Graphical abstract

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Section: Discussionmentioning

confidence: 99%