Evidence map›Paper›PMID 35264205›Full record

ArticleJournal of nanobiotechnology2022

Cur@SF NPs alleviate Friedreich's ataxia in a mouse model through synergistic iron chelation and antioxidation.

Li Xu, Zichen Sun, Zhiyao Xing, Yutong Liu, Hongting Zhao, Zhongmin Tang, Yu Luo, Shuangying Hao, Kuanyu Li

Open access · goldAbstract read
In one paragraph

Article in Journal of nanobiotechnology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.7field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 27 citations in OpenAlex.

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  17. A DFX-based iron nanochelator for cancer therapy.Frontiers in bioengineering and biotechnology · 2022
    Article
  18. Perspectives on current models of Friedreich's ataxia.Frontiers in cell and developmental biology · 2022
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 5 institutions in 1 country.

Li XuJiangsu Key Laboratory of Molecular Medicine, Medical School of Nanjing University, Nanjing, 210093, China.
Zichen SunJiangsu Key Laboratory of Molecular Medicine, Medical School of Nanjing University, Nanjing, 210093, China.
Zhiyao XingJiangsu Key Laboratory of Molecular Medicine, Medical School of Nanjing University, Nanjing, 210093, China.
Yutong LiuJiangsu Key Laboratory of Molecular Medicine, Medical School of Nanjing University, Nanjing, 210093, China.
Hongting ZhaoJiangsu Key Laboratory of Molecular Medicine, Medical School of Nanjing University, Nanjing, 210093, China.
Zhongmin TangShanghai Institute of Ceramics, Chinese Academy of Sciences, Shanghai, 200050, China.
Yu LuoShanghai Engineering Technology Research Center for Pharmaceutical Intelligent Equipment, Shanghai Frontiers Science Research Center for Druggability of Cardiovascular Noncoding RNA, Institute for Frontier Medical Technology, College of Chemistry and Chemical Engineering, Shanghai University of Engineering Science, Shanghai, 201620, China.
Shuangying HaoSchool of Medicine, Henan Polytechnic University, Jiaozuo, 454003, Henan, China. shuangying9088@hpu.edu.cn.
Kuanyu LiJiangsu Key Laboratory of Molecular Medicine, Medical School of Nanjing University, Nanjing, 210093, China. likuanyu@nju.edu.cn.ORCID http://orcid.org/0000-0001-9738-049X
Nanjing University · CNChina Pharmaceutical University · CNChinese Academy of Sciences · CNHenan Polytechnic University · CNShanghai University · CN

Funding

The National Natural Science Foundation of China 31371060The National Natural Science Foundation of China Grants #31871201The Science and Technology Project of Henan Province of China No. 202102310222The Science and Technology Project of Henan Province of China No. 202102310419
6 · The paper itself

Abstract

Abnormal iron metabolism, mitochondrial dysfunction and the derived oxidative damage are the main pathogeneses of Friedrich's ataxia (FRDA), a single-gene inherited recessive neurodegenerative disease characterized by progressive cerebellar and sensory ataxia. This disease is caused by frataxin (FXN) mutation, which reduces FXN expression and impairs iron sulfur cluster biogenesis. To date, there is no effective therapy to treat this condition. Curcumin is proposed harboring excellent ability to resist oxidative stress through Nrf2 activation and its newly found ability to chelate iron. However, its limitation is its poor water solubility and permeability. Here, we synthesized slow-release nanoparticles (NPs) by loading curcumin (Cur) into silk fibroin (SF) to form NPs with an average size of 150 nm (Cur@SF NPs), which exhibited satisfactory therapeutic effects on the improvement of FRDA manifestation in lymphoblasts (1 μM) derived from FRDA patients and in YG8R mice (150 mg/kg/5 days). Cur@SF NPs not only removed iron from the heart and diminished oxidative stress in general but also potentiate iron-sulfur cluster biogenesis, which compensates FXN deficiency to improve the morphology and function of mitochondria. Cur@SF NPs showed a significant advantage in neuron and myocardial function, thereby improving FRDA mouse behavior scores. These data encourage us to propose that Cur@SF NPs are a promising therapeutic compound in the application of FRDA disease.

Indexed as

CurcuminFibroinsFriedreich AtaxiaNanoparticlesNeurodegenerative DiseasesAnimalsAntioxidantsHumansIron Chelating AgentsMiceAntioxidantsCurcuminFibroinsIron Chelating AgentsCurcuminDrug deliveryFRDAMitochondrial functionSilk fibroin

Identifiers

PMID35264205
PMCPMC8905737
OpenAlexW4220744626

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.