The Impact of Mitochondrial Dysfunction in Amyotrophic Lateral Sclerosis
Jiantao Zhao,
Xuemei Wang,
Zijun Huo,
Yanchun Chen,
Jinmeng Liu,
Zhenhan Zhao,
Fandi Meng,
Qi Su,
Weiwei Bao,
Lingyun Zhang,
Shuang Wen,
Xin Wang,
Huancai Liu,
Shuanhu Zhou
Affiliations
Jiantao Zhao
Department of Histology and Embryology, School of Basic Medical Sciences, Weifang Medical University, Weifang 261053, China
Xuemei Wang
Department of Histology and Embryology, School of Basic Medical Sciences, Weifang Medical University, Weifang 261053, China
Zijun Huo
Department of Histology and Embryology, School of Basic Medical Sciences, Weifang Medical University, Weifang 261053, China
Yanchun Chen
Department of Histology and Embryology, School of Basic Medical Sciences, Weifang Medical University, Weifang 261053, China
Jinmeng Liu
Neurologic Disorders and Regenerative Repair Laboratory, Weifang Medical University, Weifang 261053, China
Zhenhan Zhao
Department of Histology and Embryology, School of Basic Medical Sciences, Weifang Medical University, Weifang 261053, China
Fandi Meng
Department of Histology and Embryology, School of Basic Medical Sciences, Weifang Medical University, Weifang 261053, China
Qi Su
Department of Histology and Embryology, School of Basic Medical Sciences, Weifang Medical University, Weifang 261053, China
Weiwei Bao
Department of Histology and Embryology, School of Basic Medical Sciences, Weifang Medical University, Weifang 261053, China
Lingyun Zhang
Neurologic Disorders and Regenerative Repair Laboratory, Weifang Medical University, Weifang 261053, China
Shuang Wen
Department of Joint Surgery, Affiliated Hospital of Weifang Medical University, School of Clinical Medicine, Weifang Medical University, Weifang 261061, China
Xin Wang
Department of Neurosurgery, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115, USA
Huancai Liu
Department of Joint Surgery, Affiliated Hospital of Weifang Medical University, School of Clinical Medicine, Weifang Medical University, Weifang 261061, China
Shuanhu Zhou
Department of Orthopedic Surgery, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA 02115, USA
Amyotrophic lateral sclerosis (ALS) is a rapidly progressive and highly fatal neurodegenerative disease. Although the pathogenesis of ALS remains unclear, increasing evidence suggests that a key contributing factor is mitochondrial dysfunction. Mitochondria are organelles in eukaryotic cells responsible for bioenergy production, cellular metabolism, signal transduction, calcium homeostasis, and immune responses and the stability of their function plays a crucial role in neurons. A single disorder or defect in mitochondrial function can lead to pathological changes in cells, such as an impaired calcium buffer period, excessive generation of free radicals, increased mitochondrial membrane permeability, and oxidative stress (OS). Recent research has also shown that these mitochondrial dysfunctions are also associated with pathological changes in ALS and are believed to be commonly involved in the pathogenesis of the disease. This article reviews the latest research on mitochondrial dysfunction and its impact on the progression of ALS, with specific attention to the potential of novel therapeutic strategies targeting mitochondrial dysfunction.
