Publications by authors named "Hiroko Deguchi Miyamoto"
Article Synopsis
- Ferroptosis, an iron-dependent cell death process, plays a significant role in myocardial ischemia-reperfusion injury, prompting researchers to explore the potential of deferasirox, an iron chelator, as a treatment.
- In cell cultures and mouse models, deferasirox effectively reduced iron overload, lipid peroxidation, and instances of ferroptosis, demonstrating a capacity to protect heart cells from damage post-injury.
- The combination of deferasirox and cyclosporine A (CsA) resulted in a synergistic effect, reducing infarct size and improving cardiac remodeling more effectively than either treatment alone, suggesting a promising clinical approach for managing ischemic heart damage.
Article Synopsis
- Doxorubicin-induced cardiomyopathy is a serious condition with a poor prognosis, linked to inflammation of the heart muscle.
- Research shows that activating invariant natural killer T (iNKT) cells using α-galactosylceramide can reduce heart cell death and improve heart function affected by doxorubicin.
- The study highlights that the protective effects of iNKT cells are mediated through the IFN-γ-STAT1-ERK signaling pathway, which is crucial in countering the negative effects of doxorubicin.
Article Synopsis
- Cardiac autoantibodies (cAAbs) are linked to worsening heart conditions after heart failure, but research is limited due to the lack of suitable animal models.
- Researchers created a mouse model to study cAAbs following a heart attack, focusing on their effects on cardiac function, inflammation, and fibrosis.
- The study found that cAAb-positive mice faced worse heart remodeling and prognosis, but treatment with rapamycin reduced cAAb levels and improved heart function and survival rates.
Background: Mitochondrial DNA (mtDNA)-induced myocardial inflammation is intimately involved in cardiac remodeling. ZBP1 (Z-DNA binding protein 1) is a pattern recognition receptor positively regulating inflammation in response to mtDNA in inflammatory cells, fibroblasts, and endothelial cells. However, the role of ZBP1 in myocardial inflammation and cardiac remodeling remains unclear.
View Article and Find Full Text PDFClinical use of doxorubicin (DOX) is limited because of its cardiotoxicity, referred to as DOX-induced cardiomyopathy (DIC). Mitochondria-dependent ferroptosis, which is triggered by iron overload and excessive lipid peroxidation, plays a pivotal role in the progression of DIC. Here, we showed that DOX accumulated in mitochondria by intercalating into mitochondrial DNA (mtDNA), inducing ferroptosis in an mtDNA content-dependent manner.
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- - Ischemia-reperfusion (I/R) injury is a critical area for improving recovery after heart attacks, with ferroptosis—cell death caused by iron overload and lipid peroxides—playing a key role that is not fully understood.
- - Glutathione peroxidase 4 (GPx4) acts as an important protector against ferroptosis; its reduction increases susceptibility to I/R damage, highlighting the need for therapies targeting both ferroptosis and another type of cell death called mitochondrial permeability transition (MPT).
- - The study reveals that heme oxygenase 1 activation during hypoxia contributes to iron overload and ferroptosis, distinguishing it from MPT-driven damage, suggesting that combining drugs
Doxorubicin (DOX) is an effective anti-cancer agent for various malignancies. Nevertheless, it has a side effect of cardiotoxicity, referred to as doxorubicin-induced cardiomyopathy (DIC), that is associated with a poorer prognosis. This cardiotoxicity limits the clinical use of DOX as a therapeutic agent for malignancies.
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- Apoptosis significantly contributes to cardiac rupture following a myocardial infarction (MI), with p53 being a crucial player in this process, while Hif-1α is identified as a key inducer of p53 in hypoxic conditions.
- In experiments involving mice and rat cardiomyocytes, increased levels of Hif-1α and p53 were linked to cell death, and blocking these proteins reduced apoptosis significantly.
- Cardiac-specific Hif-1α knockout mice showed lower levels of apoptosis, inflammation, and improved survival rates after MI, indicating that targeting Hif-1α could be a potential strategy for reducing cardiac rupture.
Article Synopsis
- Cardiac rupture is a severe complication following a heart attack (myocardial infarction), and high heart rate (HR) increases the risk of this condition.
- A study was conducted using mice with induced heart attacks, testing the effect of ivabradine (IVA) on HR and its impact on cardiac rupture and survival.
- The results showed that IVA significantly lowered HR, reduced cardiac rupture rates, and improved survival without affecting blood pressure or infarct size.