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Review
. 2022 May 18:14:830346.
doi: 10.3389/fnagi.2022.830346. eCollection 2022.

Adipose-Derived Mesenchymal Stem Cells Combined With Extracellular Vesicles May Improve Amyotrophic Lateral Sclerosis

Xichen Wang  1 , Yong Zhang  1 , Tian Jin  1 , Benson O A Botchway  2 , Ruihua Fan  1   3 , Lvxia Wang  1   3 , Xuehong Liu  1
Affiliations
Review

Adipose-Derived Mesenchymal Stem Cells Combined With Extracellular Vesicles May Improve Amyotrophic Lateral Sclerosis

Xichen Wang et al. Front Aging Neurosci. .

Abstract

The complexity of central nervous system diseases together with their intricate pathogenesis complicate the establishment of effective treatment strategies. Presently, the superiority of adipose-derived mesenchymal stem cells (ADSCs) on neuronal injuries has attracted significant attention. Similarly, extracellular vesicles (EVs) are potential interventional agents that could identify and treat nerve injuries. Herein, we reviewed the potential effects of ADSCs and EVs on amyotrophic lateral sclerosis (ALS) injured nerves, and expound on their practical application in the clinic setting. This article predominantly focused on the therapeutic role of ADSCs concerning the pathogenesis of ALS, the protective and reparative effects of EVs on nerve injury, as well as the impact following the combined usage of ADSCs and EVs in ALS.

Keywords: adipose-derived mesenchymal stem cells; amyotrophic lateral sclerosis; combinational therapy; extracellular vesicles; neuronal injury.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

FIGURE 1
FIGURE 1
Schematic diagram of the activation of antioxidant stress signal pathway, Keap1/Nrf2/HO-1. IL-6 can bind to membrane surface receptors and activate p62 to bind to Keap1, thereby inhibiting the binding of Keap1 to Nrf2. Subsequently, keap1-Nrf2 complex releases Nrf2 to enter the nucleus and promote the expression of HO-1 and SQSTM1. HO-1 can inhibit inflammation and oxidative stress, and reduce endoplasmic reticulum stress by inhibiting ROS/RNS pathway. SQSTM1 can inhibit keap1-Nrf2 complex to result in releasing Nrf2 and form a positive feedback.
FIGURE 2
FIGURE 2
The administration of EVs. EVs delivered intranasally bypass the BBB, and enter the brain directly through the trigeminal and olfactory nerves. Further, some EVs enter the systemic circulation, and permeates the brain through the BBB.
See this image and copyright information in PMC

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