lncRNA NEAT1: Key player in neurodegenerative diseases DOI Creative Commons
Kun Li, Ziqiang Wang

Ageing Research Reviews, Год журнала: 2023, Номер 86, С. 101878 - 101878

Опубликована: Фев. 3, 2023

Neurodegenerative diseases are the most common causes of disability worldwide. Given their high prevalence, devastating symptoms, and lack definitive diagnostic tests, there is an urgent need to identify potential biomarkers new therapeutic targets. Long non-coding RNAs (lncRNAs) have recently emerged as powerful regulatory molecules in neurodegenerative diseases. Among them, lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) has been reported be upregulated Alzheimer's disease (AD), Parkinson's (PD), Huntington's (HD), amyotrophic lateral sclerosis (ALS). However, whether this part a protective or harmful mechanism still unclear. This review summarizes our current knowledge role NEAT1 its association with characteristic aggregation misfolded proteins: amyloid-β tau AD, α-synuclein PD, mutant huntingtin HD, TAR DNA-binding protein-43 fused sarcoma/translocated liposarcoma ALS. The aim stimulate further research on more precise effective treatments for

Язык: Английский

Nucleic acid nanoassembly-enhanced RNA therapeutics and diagnosis DOI Creative Commons
Mengnan Zhao, Rujing Wang,

Kunmeng Yang

и другие.

Acta Pharmaceutica Sinica B, Год журнала: 2022, Номер 13(3), С. 916 - 941

Опубликована: Окт. 27, 2022

RNAs are involved in the crucial processes of disease progression and have emerged as powerful therapeutic targets diagnostic biomarkers. However, efficient delivery RNA to targeted location precise detection markers remains challenging. Recently, more attention has been paid applying nucleic acid nanoassemblies diagnosing treating. Due flexibility deformability acids, could be fabricated with different shapes structures. With hybridization, nanoassemblies, including DNA nanostructures, can applied enhance therapeutics diagnosis. This review briefly introduces construction properties their applications for therapy diagnosis makes further prospects development.

Язык: Английский

Процитировано

84

RNAi-based drug design: considerations and future directions DOI
Qi Tang, Anastasia Khvorova

Nature Reviews Drug Discovery, Год журнала: 2024, Номер 23(5), С. 341 - 364

Опубликована: Апрель 3, 2024

Язык: Английский

Процитировано

71

Non-coding RNA-based regulation of inflammation DOI
Milad Ashrafizadeh, Ali Zarrabi, Ebrahim Mostafavi

и другие.

Seminars in Immunology, Год журнала: 2022, Номер 59, С. 101606 - 101606

Опубликована: Янв. 1, 2022

Язык: Английский

Процитировано

70

Amplifying gene expression with RNA-targeted therapeutics DOI Open Access
Olga Khorkova, Jack Stahl,

Aswathy Joji

и другие.

Nature Reviews Drug Discovery, Год журнала: 2023, Номер 22(7), С. 539 - 561

Опубликована: Май 30, 2023

Язык: Английский

Процитировано

69

lncRNA NEAT1: Key player in neurodegenerative diseases DOI Creative Commons
Kun Li, Ziqiang Wang

Ageing Research Reviews, Год журнала: 2023, Номер 86, С. 101878 - 101878

Опубликована: Фев. 3, 2023

Neurodegenerative diseases are the most common causes of disability worldwide. Given their high prevalence, devastating symptoms, and lack definitive diagnostic tests, there is an urgent need to identify potential biomarkers new therapeutic targets. Long non-coding RNAs (lncRNAs) have recently emerged as powerful regulatory molecules in neurodegenerative diseases. Among them, lncRNA nuclear paraspeckle assembly transcript 1 (NEAT1) has been reported be upregulated Alzheimer's disease (AD), Parkinson's (PD), Huntington's (HD), amyotrophic lateral sclerosis (ALS). However, whether this part a protective or harmful mechanism still unclear. This review summarizes our current knowledge role NEAT1 its association with characteristic aggregation misfolded proteins: amyloid-β tau AD, α-synuclein PD, mutant huntingtin HD, TAR DNA-binding protein-43 fused sarcoma/translocated liposarcoma ALS. The aim stimulate further research on more precise effective treatments for

Язык: Английский

Процитировано

68