Non-coding RNAs in Ischemic Stroke: Roles in the Neuroinflammation and Cell Death

  • PDF / 959,864 Bytes
  • 15 Pages / 595.276 x 790.866 pts Page_size
  • 28 Downloads / 191 Views

DOWNLOAD

REPORT


REVIEW ARTICLE

Non-coding RNAs in Ischemic Stroke: Roles in the Neuroinflammation and Cell Death Meng Lu 1,2 & Xingang Dong 3 & Zhenqiang Zhang 1 & Weifeng Li 4 & Seyed Esmaeil Khoshnam 5 Received: 17 March 2020 / Revised: 10 May 2020 / Accepted: 7 June 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020

Abstract Ischemic stroke is one of the leading causes of death and long-term disability worldwide. As an important class of pervasive genes involved in many pathophysiological processes of ischemic stroke, non-coding RNAs (ncRNAs) have received attention in the past decades. ncRNAs are a class of functional RNAs that regulate gene expression in a post-transcriptional manner, and including microRNAs, long non-coding RNAs, and circular RNAs. Several studies have deciphered that ncRNAs have a key role in the ischemic stroke-induced neuroinflammation and cell death via different molecules and pathways. Thus, ncRNAs show great promise as novel molecular targets in ischemic stroke. In this article, we provide an updated review of the current state of our knowledge about the roles of different types of ncRNAs in neuroinflammation and cell death following ischemic stroke, which may facilitate the translation of ncRNAs research into clinical practice to improve the clinical outcome of stroke therapy. Keywords Non-coding RNAs . Ischemic stroke . Cell death . Neuroinflammation

Introduction Stroke is a life-threatening disease and a leading cause of death and long-term disability worldwide. Ischemic stroke is caused by a sudden reduction of cerebral blood flow with a subsequent lack of oxygen and glucose, which are needed to maintain energy-dependent processes in neuronal cells. Ischemic stroke ultimately leads to impairment or loss of neurological function, neuronal cell death, and brain infarction (He et al. 2019; Khoshnam et al. 2017d). Numerous efforts

* Weifeng Li [email protected] * Seyed Esmaeil Khoshnam [email protected] 1

Academy of Traditional Chinese Medicine, Henan University of Chinese Medicine, Zhengzhou 450046, China

2

College of Integration of Chinese and Western Medicine, Hebei University of Chinese Medicine, Shijiazhuang 050200, China

3

Frist Clinical Medical College, Henan University of Chinese Medicine, Zhengzhou 450008, China

4

Third Clinical Medical College, Henan University of Chinese Medicine, Zhengzhou 450008, China

5

Physiology Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran

have been made to restore neurological function and reduce ischemia-induced neuronal injury, but effective therapies are limited for several reasons, including the rapid development of cerebral damage during ischemia, complex interactions between signaling pathways, and the limited therapeutic window (Yin et al. 2010). For instance, the approved therapies for acute ischemic stroke are a clot retrieval device as a first-line treatment, along with intravenous recombinant tissue plasminogen activators (r-tPAs). However, this treatment is limited by its