The intimate partner violence (IPV) targeting women is an escalating concern worldwide. Despite the widespread presence of IPV, its impact on women’s pathophysiology is poorly understood. In this study, we tried to unveil the mechanisms behind cardiac pathophysiology related to IPV. Using a mouse model resembling an IPV scenario, we uncovered some significant biomarkers related to cardiac dysfunction produced by reiterated male-to-female violent interaction (RMFVI). A substantial increase in collagen fibers was observed through trichrome staining, suggesting the development of cardiac interstitial and perivascular fibrosis due to IPV. RNA transcriptomics was then performed to investigate suspicious biomarkers. The detected biomarkers displayed alignment with cardiac dysfunction. Cytochrome c, related to myocyte loss, was upregulated, strengthening the finding of fibrosis by trichrome staining. Downregulation of BDNF, upregulation of Alpha-synuclein, and Monoamine Oxidase B (MAO-B) were other significant biomarkers that are all parallel to increased cardiac stress and vulnerability to damage. Thereby, RMFVI endangers cardiac homeostasis, inducing fibrosis and ultimately leading to heart failure.
The intimate partner violence (IPV) targeting women is an escalating concern worldwide. Despite the widespread presence of IPV, its impact on women’s pathophysiology is poorly understood. In this study, we tried to unveil the mechanisms behind cardiac pathophysiology related to IPV. Using a mouse model resembling an IPV scenario, we uncovered some significant biomarkers related to cardiac dysfunction produced by reiterated male-to-female violent interaction (RMFVI). A substantial increase in collagen fibers was observed through trichrome staining, suggesting the development of cardiac interstitial and perivascular fibrosis due to IPV. RNA transcriptomics was then performed to investigate suspicious biomarkers. The detected biomarkers displayed alignment with cardiac dysfunction. Cytochrome c, related to myocyte loss, was upregulated, strengthening the finding of fibrosis by trichrome staining. Downregulation of BDNF, upregulation of Alpha-synuclein, and Monoamine Oxidase B (MAO-B) were other significant biomarkers that are all parallel to increased cardiac stress and vulnerability to damage. Thereby, RMFVI endangers cardiac homeostasis, inducing fibrosis and ultimately leading to heart failure.
Identification of significant biomarkers associated with heart pathophysiology in female mice subjected to male-to-female violence.
KIM, YERIN
2024/2025
Abstract
The intimate partner violence (IPV) targeting women is an escalating concern worldwide. Despite the widespread presence of IPV, its impact on women’s pathophysiology is poorly understood. In this study, we tried to unveil the mechanisms behind cardiac pathophysiology related to IPV. Using a mouse model resembling an IPV scenario, we uncovered some significant biomarkers related to cardiac dysfunction produced by reiterated male-to-female violent interaction (RMFVI). A substantial increase in collagen fibers was observed through trichrome staining, suggesting the development of cardiac interstitial and perivascular fibrosis due to IPV. RNA transcriptomics was then performed to investigate suspicious biomarkers. The detected biomarkers displayed alignment with cardiac dysfunction. Cytochrome c, related to myocyte loss, was upregulated, strengthening the finding of fibrosis by trichrome staining. Downregulation of BDNF, upregulation of Alpha-synuclein, and Monoamine Oxidase B (MAO-B) were other significant biomarkers that are all parallel to increased cardiac stress and vulnerability to damage. Thereby, RMFVI endangers cardiac homeostasis, inducing fibrosis and ultimately leading to heart failure.| File | Dimensione | Formato | |
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https://hdl.handle.net/20.500.12608/89544