Cobaltosic oxide-polyethylene glycol-triphenylphosphine nanoparticles ameliorate the acute-to-chronic kidney disease transition by inducing BNIP3-mediated mitophagy

Qin, Shaozong; Liu, Chi; Chen, Yin; Yao, Mengying; Liao, Shu‐Yi; Wang, Xin; Gong, Shuiqin; Guan, Xu; Li, Yan; Xiong, Jiachuan; Chen, Jing; Shen, Yanjie; Liu, Yong; Zhao, Jinghong; Huang, Yinghui

doi:10.1016/j.kint.2023.01.025

Cited by 10 publications

(8 citation statements)

References 48 publications

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“…E) COPT ameliorated the acute-to-chronic kidney disease transition by inducing BNIP3-mediated mitophagy.Reproduced with permission. [211] Copyright 2023, International Society of Nephrolohy. Some nanomedicines that promote mitochondrial production have also been developed for the treatment of related diseases.…”

Section: Supplementing Mitochondrial Contentsmentioning

confidence: 99%

“…[292] Polymeric NPs containing formoterol recovered mitochondrial number and protein in the renal cortex and reduced tubular necrosis. [128] Recently, Duan et al demonstrated that a roper delay ironreplenishing therapy can significantly enhance the anti-AKI Active ingredient AKI Atv/PTP-TCeria NPs [ 55] -TPP 37.5 ± 2.62 −1.72 ± 0.433 Atorvastatin; Ceria NPs AKI IL-10 + EVs [ 207] EVs -134 -IL-10 AKI FNPs [ 128] --4 6 3 ± 40 -Formoterol AKI Fe 3 O 4 @NMN nanoprobes [ 293] NMN -3.4 26 NMN AKI SS-31 NPs [ 290] Hyaluronic acid targets CD44 SS-31 53 ± 0.17 -19.6 ± 0.7 SS-31 AKI MSC-Evs [ 227] --≈160 -miRNA200a-3p AKI nHA/PLBR [183] Hyaluronic acid -226.9 ± 4.5 -23.9 ± 0.2 Bilirubin AKI tFNA-Typ complex (TTC) [294] -16.93 ± 3.727 -9.74 ± 3.71 Typhaneoside AKI mSiO2@BA-AM/BAC@LTH NPs [ 295] Renal tubule-targeting peptide PEG-LTH -78.8 -13.3 BAPTA (Ca 2+ -selective chelator) AKI FNC/Cur [ 296] Ferritin -14 -17 ± 0.97 Curcumin AKI GA-NPs [ 297] --≈4.5 -Gambogic acid Chronic kidney disease COPT [211] --55.8 19.4 ± 2.01 Cobaltosic oxide Diabetic kidney disease Ad@Gel [ 292] --≈10 -Adropin…”

Section: Ischemic Strokementioning

confidence: 99%

“…Cobaltosic oxide‐polyethylene glycol‐triphenylphosphine (COPT) NPs were proven to dose‐dependently induce the expression of BNIP3 thus restoring mitophagy flux and protecting mitochondria (Figure 11E). [ 211 ]…”

Section: Nanodrug‐mediate Therapeutic Strategies To Mitochondrial Dys...mentioning

confidence: 99%

“…Copyright 2023, American Chemical Society. E) COPT ameliorated the acute-to-chronic kidney disease transition by inducing BNIP3-mediated mitophagy.Reproduced with permission [211]. Copyright 2023, International Society of Nephrolohy.…”

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confidence: 99%

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Revitalizing Ancient Mitochondria with Nano‐Strategies: Mitochondria‐Remedying Nanodrugs Concentrate on Disease Control

Long,

Liu,

Nan

et al. 2024

Advanced Materials

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Mitochondria, widely known as the energy factories of eukaryotic cells, have a myriad of vital functions across diverse cellular processes. Dysfunctions within mitochondria serve as catalysts for various diseases, prompting widespread cellular demise. Mounting research on remedying damaged mitochondria indicates that mitochondria constitute a valuable target for therapeutic intervention against diseases. But the less clinical practice and lower recovery rate imply the limitation of traditional drugs, which need a further breakthrough. Nanotechnology has approached favorable regiospecific biodistribution and high efficacy by capitalizing on excellent nanomaterials and targeting drug delivery. Mitochondria‐remedying nanodrugs have achieved ideal therapeutic effects. In this review, we have elucidated the significance of mitochondria in various cells and organs, while also compiling mortality data for related diseases. Correspondingly, nanodrug‐mediate therapeutic strategies and applicable mitochondria‐remedying nanodrugs in disease were detailed, with a full understanding of the roles of mitochondria dysfunction and the advantages of nanodrugs. In addition, the future challenges and directions have been widely discussed. In conclusion, this review provides comprehensive insights into the design and development of mitochondria‐remedying nanodrugs, aiming to help scientists who desire to extend their research fields and engage in this interdisciplinary subject.This article is protected by copyright. All rights reserved

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Section: Supplementing Mitochondrial Contentsmentioning

confidence: 99%

Section: Ischemic Strokementioning

confidence: 99%

Section: Nanodrug‐mediate Therapeutic Strategies To Mitochondrial Dys...mentioning

confidence: 99%

mentioning

confidence: 99%

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Revitalizing Ancient Mitochondria with Nano‐Strategies: Mitochondria‐Remedying Nanodrugs Concentrate on Disease Control

Long,

Liu,

Nan

et al. 2024

Advanced Materials

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show abstract

“…Therefore, a therapeutic strategy by targeting HIF-1 α and BNIP3-mediated mitophagy could alleviate renal fibrosis and delay the progression of CKD. In addition, in 2023 Qin et al. (2023) reported that COPT could reduce the expression of mtROS and fibrosis markers, reduced the occurrence of apoptosis, significantly improved AKI, and reduced kidney fibrosis in mice with CKD by inducing BNIP3 mediated mitophagy, while having good biocompatibility.…”

Section: Introductionmentioning

confidence: 99%

The role of mitophagy in the development of chronic kidney disease

Yang,

Li,

Geng

et al. 2024

PeerJ

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Chronic kidney disease (CKD) represents a significant global health concern, with renal fibrosis emerging as a prevalent and ultimate manifestation of this condition. The absence of targeted therapies presents an ongoing and substantial challenge. Accumulating evidence suggests that the integrity and functionality of mitochondria within renal tubular epithelial cells (RTECs) often become compromised during CKD development, playing a pivotal role in the progression of renal fibrosis. Mitophagy, a specific form of autophagy, assumes responsibility for eliminating damaged mitochondria to uphold mitochondrial equilibrium. Dysregulated mitophagy not only correlates with disrupted mitochondrial dynamics but also contributes to the advancement of renal fibrosis in CKD. While numerous studies have examined mitochondrial metabolism, ROS (reactive oxygen species) production, inflammation, and apoptosis in kidney diseases, the precise pathogenic mechanisms underlying mitophagy in CKD remain elusive. The exact mechanisms through which modulating mitophagy mitigates renal fibrosis, as well as its influence on CKD progression and prognosis, have not undergone systematic investigation. The role of mitophagy in AKI has been relatively clear, but the role of mitophagy in CKD is still rare. This article presents a comprehensive review of the current state of research on regulating mitophagy as a potential treatment for CKD. The objective is to provide fresh perspectives, viable strategies, and practical insights into CKD therapy, thereby contributing to the enhancement of human living conditions and patient well-being.

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Self‐Assembling P38 Peptide Inhibitor Nanoparticles Ameliorate the Transition from Acute to Chronic Kidney Disease by Suppressing Ferroptosis

Xin,

Gong,

Chen

et al. 2024

Adv Healthcare Materials

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Accumulating evidence highlights p38 as a crucial factor highly activated during the process of acute kidney injury (AKI), but the application of p38 inhibitor in AKI was quite limited due to the low efficiency and poor kidney‐targeting ability. Herein, a novel self‐assembling peptide nanoparticle with specific p38‐inhibiting activity was constructed, which linked mitogen‐activated protein kinase kinase 3b (MKK3b), the functional domain of p38, with the cell‐penetrating TAT sequence, ultimately self‐assembling into TAT‐MKK3b nanoparticles (TMNPs) through tyrosinase oxidation. Subsequent in vitro and in vivo studies demonstrated that TMNPs preferably accumulated in the renal tubular epithelial cells (RTECs) through forming protein coronas by binding to albumin, and strongly improved the reduced renal function of ischemia‐reperfusion injury (IRI)‐induced AKI and its transition to chronic kidney disease (CKD). Mechanically, TMNPs inhibited ferroptosis via its solute carrier family 7 member 11 (SLC7A11)/glutathione peroxidase 4 (GPX4) axis‐inducing capacity and synergistic potent antioxidant property in AKI. Our findings indicated that the multifunctional TMNPs exhibited renal targeting, ROS‐scavenging and ferroptosis‐mitigating capabilities, which may serve as a promising therapeutic agent for the treatment of AKI and its progression to CKD.This article is protected by copyright. All rights reserved

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Cobaltosic oxide-polyethylene glycol-triphenylphosphine nanoparticles ameliorate the acute-to-chronic kidney disease transition by inducing BNIP3-mediated mitophagy

Cited by 10 publications

References 48 publications

Revitalizing Ancient Mitochondria with Nano‐Strategies: Mitochondria‐Remedying Nanodrugs Concentrate on Disease Control

Revitalizing Ancient Mitochondria with Nano‐Strategies: Mitochondria‐Remedying Nanodrugs Concentrate on Disease Control

The role of mitophagy in the development of chronic kidney disease

Self‐Assembling P38 Peptide Inhibitor Nanoparticles Ameliorate the Transition from Acute to Chronic Kidney Disease by Suppressing Ferroptosis

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