Melanin nanoparticles alleviate sepsis-induced myocardial injury by suppressing ferroptosis and inflammation

Liu, Chang; Zou, Quan; Tang, Huixin; Liu, Jia; Zhang, Shiqi; Fan, Caihong; Zhang, Junwei; Liu, Ruiqing; Liu, Yashan; Liu, Ruiyan; Zhao, Yan; Wu, Qiang; Qi, Zhi; Shen, Yanna

doi:10.1016/j.bioactmat.2022.12.026

Cited by 27 publications

(11 citation statements)

References 41 publications

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“…found that melanin nanoparticles alleviated sepsis-induced myocardial injury by suppressing ferroptosis and inflammation caused by melanin-like nanoparticles. 29 Consequently, PPR may exert strong anti-ROS effects. To verify this prediction, HK-2 cells were divided into four groups, including a control, stimulated (LPS), PP, and PPR group, and DCFH-DA was used to label ROS.…”

Section: Resultsmentioning

confidence: 99%

Melanin-like nanoparticles alleviate ischemia-reperfusion injury in the kidney by scavenging reactive oxygen species and inhibiting ferroptosis

Feng,

Zhu,

Xia

et al. 2024

iScience

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Section: Resultsmentioning

confidence: 99%

Melanin-like nanoparticles alleviate ischemia-reperfusion injury in the kidney by scavenging reactive oxygen species and inhibiting ferroptosis

Feng,

Zhu,

Xia

et al. 2024

iScience

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“…A sepsis murine model was developed by LPS intraperitoneal injection (10 mg/kg) as reported . For in vivo potency assay, the mice were administered with LPS with or without BR formulations.…”

Section: Methodsmentioning

confidence: 99%

“…A sepsis murine model was developed by LPS intraperitoneal injection (10 mg/kg) as reported. 20 For in vivo potency assay, the mice were administered with LPS with or without BR formulations. The impact of BRNP on a sepsis-induced ALI was assessed by dividing the mice into three experimental groups (n = 8): the control group, the LPS group, and the LPS + BRNP group (0.5, 1, and 2.5 mg/kg, intraperitoneally).…”

Section: T H Imentioning

confidence: 99%

Bilirubin Nanoparticles Alleviate Sepsis-Induced Acute Lung Injury by Protecting Pulmonary Endothelia Glycocalyx and Reducing Inflammation

Xia,

Sun,

Zhao

et al. 2024

ACS Appl. Nano Mater.

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Acute lung injury (ALI) remains one of the most common complications of sepsis. Although many potential effective pharmacologic and ventilatory treatment strategies have been reported, there is still a lack of effective means of treatment of sepsis-induced ALI in the clinic. The aim of this study is to develop an easy-made endogenous bilirubin nanoparticle (BRNP) that could treat sepsis-induced ALI and investigate its underlying therapeutic mechanism. We prepared BRNP by bilirubin (BR) selfassembly and bovine serum albumin (BSA) coating with a simple one-pot nanoprecipitation method. BRNP holds good physical stability and could release BR in a sustained manner in a neutral medium but initiate a burst release in either acidic or oxidative conditions. In a sepsis murine model, BRNP could substantially alleviate the sepsis-induced lung injury, as evidenced by reduced histopathological changes of lung tissues and also reduced inflammation development. Mechanically, BRNP could alleviate the glycocalyx damage, inhibit the NF-κB pathway, and reduce proinflammatory factor release in vivo. This study provides a simple and robust BRNP to treat sepsis-induced ALI, which may pave the way to design multifunctional nanomedicine for clinical translation.

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“…MMPP protects the heart against sepsis-induced myocardial injury by inhibiting ferroptosis and inflammation and might be a novel therapeutic approach in the future (Liu et al 2023 ). Ferroptosis is a novel mechanism for ZnONP-induced endothelial cytotoxicity, and NCOA4-mediated ferritinophagy is required for ZnONP-induced ferroptotic cell death (Qin et al 2021 ).…”

Section: Nanomaterialsmentioning

confidence: 99%

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

Fang,

Xie,

Deng

2024

Cell Biol Toxicol

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

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Melanin nanoparticles alleviate sepsis-induced myocardial injury by suppressing ferroptosis and inflammation

Cited by 27 publications

References 41 publications

Melanin-like nanoparticles alleviate ischemia-reperfusion injury in the kidney by scavenging reactive oxygen species and inhibiting ferroptosis

Melanin-like nanoparticles alleviate ischemia-reperfusion injury in the kidney by scavenging reactive oxygen species and inhibiting ferroptosis

Bilirubin Nanoparticles Alleviate Sepsis-Induced Acute Lung Injury by Protecting Pulmonary Endothelia Glycocalyx and Reducing Inflammation

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

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