Axonal Pathology: From Cellular Mechanism to Therapy Targets

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: closed (15 June 2023) | Viewed by 6526

Special Issue Editor


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Guest Editor
Department of Life Sciences, National Cheng Kung University, Tainan 70101, Taiwan
Interests: axonal transport; ubiquitin-proteasome system; autophagy-lysosome system; mitochondrial dysfunction

Special Issue Information

Dear Colleagues,

Loss of neurons represents the pathological event in neurodegenerative diseases. In the nervous system, axons convey the communication between neurons. The great sizes of axons make them vulnerable to various insults. Thus far, the majority of studies for potential mechanisms and therapeutic targets for neurodegenerative disorders have focused on events that occur in the cell bodies of neurons. However, white matter defects have been identified as an early neuropathological event, leading to axonal degeneration and eventual death of neurons in many neurodegenerative diseases.

Therefore, we invite authors to submit original research and review articles that focus on the molecular mechanisms and therapeutic potential of axonal pathology. Potential topics include but are not limited to:

  • Dystrophic neurite/axonal degeneration
  • Cytoskeleton integrity
  • Microtubule-based transport
  • Ubiquitin–proteasome system
  • Autophagy–lysosome system
  • Growth factor signaling
  • Mitochondria

Dr. Lu-Shiun Her
Guest Editor

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Keywords

  • dystrophic neurite
  • microtubule-based transport
  • ubiquitin-proteasome system
  • autophagy-lysosome system
  • mitochondria

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Published Papers (1 paper)

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Review

32 pages, 12376 KiB  
Review
Axonal Regeneration: Underlying Molecular Mechanisms and Potential Therapeutic Targets
by Rabia Akram, Haseeb Anwar, Muhammad Shahid Javed, Azhar Rasul, Ali Imran, Shoaib Ahmad Malik, Chand Raza, Ikram Ullah Khan, Faiqa Sajid, Tehreem Iman, Tao Sun, Hyung Soo Han and Ghulam Hussain
Biomedicines 2022, 10(12), 3186; https://doi.org/10.3390/biomedicines10123186 - 8 Dec 2022
Cited by 22 | Viewed by 6191
Abstract
Axons in the peripheral nervous system have the ability to repair themselves after damage, whereas axons in the central nervous system are unable to do so. A common and important characteristic of damage to the spinal cord, brain, and peripheral nerves is the [...] Read more.
Axons in the peripheral nervous system have the ability to repair themselves after damage, whereas axons in the central nervous system are unable to do so. A common and important characteristic of damage to the spinal cord, brain, and peripheral nerves is the disruption of axonal regrowth. Interestingly, intrinsic growth factors play a significant role in the axonal regeneration of injured nerves. Various factors such as proteomic profile, microtubule stability, ribosomal location, and signalling pathways mark a line between the central and peripheral axons’ capacity for self-renewal. Unfortunately, glial scar development, myelin-associated inhibitor molecules, lack of neurotrophic factors, and inflammatory reactions are among the factors that restrict axonal regeneration. Molecular pathways such as cAMP, MAPK, JAK/STAT, ATF3/CREB, BMP/SMAD, AKT/mTORC1/p70S6K, PI3K/AKT, GSK-3β/CLASP, BDNF/Trk, Ras/ERK, integrin/FAK, RhoA/ROCK/LIMK, and POSTN/integrin are activated after nerve injury and are considered significant players in axonal regeneration. In addition to the aforementioned pathways, growth factors, microRNAs, and astrocytes are also commendable participants in regeneration. In this review, we discuss the detailed mechanism of each pathway along with key players that can be potentially valuable targets to help achieve quick axonal healing. We also identify the prospective targets that could help close knowledge gaps in the molecular pathways underlying regeneration and shed light on the creation of more powerful strategies to encourage axonal regeneration after nervous system injury. Full article
(This article belongs to the Special Issue Axonal Pathology: From Cellular Mechanism to Therapy Targets)
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