Non-coding RNA-mediated modulation of ferroptosis in cardiovascular diseases

Biomedicine & Pharmacotherapy, Год журнала: 2023, Номер 164, С. 114993 - 114993

Опубликована: Июнь 9, 2023

Cardiovascular disease (CVD) is a major contributor to increasing morbidity and mortality worldwide seriously threatens human health life. Cardiomyocyte death considered the pathological basis of various CVDs, including myocardial infarction, heart failure, aortic dissection. Multiple mechanisms, such as ferroptosis, necrosis, apoptosis, contribute cardiomyocyte death. Among them, ferroptosis an iron-dependent form programmed cell that plays vital role in physiological processes, from development aging immunity CVD. The dysregulation has been shown be closely associated with CVD progression, yet its underlying mechanisms are still not fully understood. In recent years, growing amount evidence suggests non-coding RNAs (ncRNAs), particularly microRNAs, long RNAs, circular involved regulation thus affecting progression. Some ncRNAs also exhibit potential value biomarker and/or therapeutic target for patients this review, we systematically summarize findings on their We focus clinical applications diagnostic prognostic biomarkers well targets treatment. DATA AVAILABILITY: No new data were created or analyzed study. Data sharing applicable article.

Язык: Английский

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Nrf2: a dark horse in doxorubicin-induced cardiotoxicity

Cell Death Discovery, Год журнала: 2023, Номер 9(1)

Опубликована: Июль 26, 2023

Abstract Being a broad-spectrum anticancer drug, doxorubicin is indispensable for clinical treatment. Unexpectedly, its cardiotoxic side effects have proven to be formidable obstacle. Numerous studies are currently devoted elucidating the pathological mechanisms underlying doxorubicin-induced cardiotoxicity. Nrf2 has always played crucial role in oxidative stress, but numerous demonstrated that it also plays vital part like cell death and inflammation. on associated with cardiotoxicity demonstrate this. Several drugs, natural synthetic compounds, as well small molecule RNAs been prevent by activating Nrf2. Consequently, this study emphasizes introduction of Nrf2, discusses cardiotoxicity, concludes summary therapeutic modalities targeting ameliorate highlighting potential value

Язык: Английский

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Idebenone alleviates doxorubicin-induced cardiotoxicity by stabilizing FSP1 to inhibit ferroptosis

Acta Pharmaceutica Sinica B, Год журнала: 2024, Номер 14(6), С. 2581 - 2597

Опубликована: Март 11, 2024

Doxorubicin (DOX)-mediated cardiotoxicity can exacerbate mortality in oncology patients, but related pharmacotherapeutic measures are relatively limited. Ferroptosis was recently identified as a major mechanism of DOX-induced cardiotoxicity. Idebenone, novel ferroptosis inhibitor, is well-described clinical drug widely used. However, its role and pathological still unclear. In this study, we demonstrated the effects idebenone on elucidated underlying mechanism. A single intraperitoneal injection DOX (15 mg/kg) administrated to establish The results showed that significantly attenuated cardiac dysfunction due ability regulate acute Fe2+ ROS overload, which resulted ferroptosis. CESTA BLI further revealed idebenone's anti-ferroptosis effect mediated by FSP1. Interestingly, increased FSP1 protein levels did not affect Fsp1 mRNA presence DOX. Idebenone could form stable hydrogen bonds with at K355, may influence association ubiquitin. confirmed stabilized inhibiting ubiquitination degradation. conclusion, study demonstrates via regulation FSP1, making it potential for patients receiving treatment.

Язык: Английский

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Ferroptosis mechanisms and regulations in cardiovascular diseases in the past, present, and future

Cell Biology and Toxicology, Год журнала: 2024, Номер 40(1)

Опубликована: Март 21, 2024

Abstract Cardiovascular diseases (CVDs) are the main that endanger human health, and their risk factors contribute to high morbidity a rate of hospitalization. Cell death is most important pathophysiology in CVDs. As one cell mechanisms, ferroptosis new form regulated (RCD) broadly participates CVDs (such as myocardial infarction, heart transplantation, atherosclerosis, failure, ischaemia/reperfusion (I/R) injury, atrial fibrillation, cardiomyopathy (radiation-induced cardiomyopathy, diabetes sepsis-induced cardiac doxorubicin-induced iron overload hypertrophic cardiomyopathy), pulmonary arterial hypertension), involving regulation, metabolic mechanism lipid peroxidation. This article reviews recent research on regulation its relationship with occurrence treatment CVDs, aiming provide ideas targets for clinical diagnosis by clarifying latest progress research. Graphical • The identification, development history characterization ferroptosis. role different subcellular organelles organelle-specific regulators includes metabolism, amino acid metabolism. cardiovascular cells diseases. efficacy pathological involved

Язык: Английский

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Ferritinophagy and ferroptosis in cardiovascular disease: Mechanisms and potential applications

Biomedicine & Pharmacotherapy, Год журнала: 2021, Номер 141, С. 111872 - 111872

Опубликована: Июль 7, 2021

Ferroptosis is a type of regulated cell death driven by iron dependent accumulation cellular reactive oxygen species (ROS) when glutathione (GSH)-dependent lipid peroxidation repair systems are compromised. Nuclear receptor co-activator 4 (NCOA4)-mediated selective autophagy ferritin, termed ferritinophagy, involves the regulation ferroptosis. Emerging evidence has revealed that ferritinophagy and ferroptosis exert significant role in occurrence development cardiovascular disease. In present review, we aimed to brief overview focusing on underlying mechanism regulations involved. We summarize discuss relevant research progress diseases accompanied with potential applications modulators treatment ferroptosis-associated diseases.

Язык: Английский

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