PM2.5-induced iron homeostasis imbalance triggers cardiac hypertrophy through ferroptosis in a selective autophagy crosstalk manner

Redox Biology, Год журнала: 2024, Номер 72, С. 103158 - 103158

Опубликована: Апрель 12, 2024

Exposure to PM2.5 is correlated with cardiac remodeling, of which hypertrophy one the main clinical manifestations. Ferroptosis plays an important role in hypertrophy. However, potential mechanism PM2.5-induced through ferroptosis remains unclear. This study aimed explore molecular caused by and intervention MitoQ involved this process. The results showed that could induce dysfunction mice. Meanwhile, characteristics were observed, such as iron homeostasis imbalance, lipid peroxidation, mitochondrial damage abnormal expression key molecules. treatment effectively mitigate these alternations. After treating human cardiomyocyte AC16 PM2.5, activator (Erastin) inhibitor (Fer-1), it was found promote ferritinophagy lead well accumulation intracellular labile iron. Subsequently, mitophagy activated provided additional source iron, enhancing sensitivity cells ferroptosis. Furthermore, Fer-1 alleviated cytotoxicity overload cytoplasm mitochondria cells. It worth noting during process ferroptosis, metabolism mediated activation a temporal order. In addition, NCOA4 knockdown reversed imbalance peroxidation thereby alleviating summary, our imbalance-mediated crosstalk played

Язык: Английский

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Apoptotic Bodies Derived from Fibroblast‐Like Cells in Subcutaneous Connective Tissue Inhibit Ferroptosis in Ischaemic Flaps via the miR‐339‐5p/KEAP1/Nrf2 Axis

Advanced Science, Год журнала: 2024, Номер 11(24)

Опубликована: Апрель 19, 2024

Abstract Preventing and treating avascular necrosis at the distal end of flaps are critical to surgery success, but current treatments not ideal. A recent study shows that apoptotic bodies (ABs) generated near site apoptosis can be taken up promote cell proliferation. The reveals ABs derived from fibroblast‐like cells in subcutaneous connective tissue (FSCT cells) skin promoted ischaemic flap survival. It is also found inhibited death oxidative stress M1‐to‐M2 polarization macrophages. Transcriptome sequencing protein level testing demonstrated survival endothelial macrophages by inhibiting ferroptosis via KEAP1‐Nrf2 axis. Furthermore, microRNA (miR) data vitro vivo experiments KEAP1 delivering miR‐339‐5p exert therapeutic effects. In conclusion, FSCT cell‐derived ferroptosis, macrophage transition miR‐339‐5p/KEAP1/Nrf2 axis These results provide a potential strategy administering ABs.

Язык: Английский

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Irisin regulates oxidative stress and mitochondrial dysfunction through the UCP2-AMPK pathway in prion diseases

Cell Death and Disease, Год журнала: 2025, Номер 16(1)

Опубликована: Фев. 3, 2025

Abstract Prion diseases are a group of fatal neurodegenerative disorders characterized by the abnormal folding cellular prion proteins into pathogenic forms. The development these is intricately linked to oxidative stress and mitochondrial dysfunction. Irisin, an endogenous myokine, has demonstrated considerable neuroprotective potential due its antioxidative properties. However, protective effects irisin against have yet be clarified. Our findings indicate that treatment with exogenous can mitigate apoptosis induced PrP 106–126. Additionally, significantly reduces alleviates dysfunction triggered 106–126 . Furthermore, targets uncoupling protein 2 (UCP2) activates AMPK-Nrf2 pathway, substantially improving in N2a cells These results suggest represents novel promising therapeutic approach for treating diseases.

Язык: Английский

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Ferroptosis: mechanism and role in diabetes-related cardiovascular diseases

Cardiovascular Diabetology, Год журнала: 2025, Номер 24(1)

Опубликована: Фев. 7, 2025

Cardiovascular diseases represent the principal cause of death and comorbidity among people with diabetes. Ferroptosis, an iron-dependent non-apoptotic regulated cellular characterized by lipid peroxidation, is involved in pathogenesis diabetic cardiovascular diseases. The susceptibility to ferroptosis hearts possibly related myocardial iron accumulation, abnormal metabolism excess oxidative stress under hyperglycemia conditions. Accumulating evidence suggests can be therapeutic target for This review summarizes ferroptosis-related mechanisms novel choices targeting pathways. Further study on ferroptosis-mediated cardiac injury enhance our understanding pathophysiology provide more potential choices.

Язык: Английский

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Ferroptosis in heart failure

Journal of Molecular and Cellular Cardiology, Год журнала: 2022, Номер 173, С. 141 - 153

Опубликована: Окт. 20, 2022

Язык: Английский

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