scholarly journals Neuroinflammatory Mechanisms of Mitochondrial Dysfunction and Neurodegeneration in Glaucoma

2021 ◽  
Vol 2021 ◽  
pp. 1-18
Author(s):  
Joao N. Duarte
Keyword(s):  
Mitochondrial Dysfunction ◽  
Autosomal Dominant ◽  
Cell Loss ◽  
Mitochondrial Damage ◽  
Retinal Ganglion ◽  
Dna Mutations ◽  
Age Related ◽  
Species Production ◽  
Molecular Patterns ◽  
Damage Associated Molecular Patterns

The exact mechanism of retinal ganglion cell loss in the pathogenesis of glaucoma is yet to be understood. Mitochondrial damage-associated molecular patterns (DAMPs) resulting from mitochondrial dysfunction have been linked to Leber’s hereditary optic neuropathy and autosomal dominant optic atrophy, as well as to brain neurodegenerative diseases. Recent evidence shows that, in conditions where mitochondria are damaged, a sustained inflammatory response and downstream pathological inflammation may ensue. Mitochondrial damage has been linked to the accumulation of age-related mitochondrial DNA mutations and mitochondrial dysfunction, possibly through aberrant reactive oxygen species production and defective mitophagy. The present review focuses on how mitochondrial dysfunction may overwhelm the ability of neurons and glial cells to adequately maintain homeostasis and how mitochondria-derived DAMPs trigger the immune system and induce neurodegeneration.

scholarly journals Mitochondrial Dysfunction and Mitophagy in Fuchs Endothelial Corneal Dystrophy

Cells ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1888
Author(s):  
Varun Kumar ◽  
Ula V. Jurkunas
Keyword(s):  
Mitochondrial Dysfunction ◽  
Treatment Options ◽  
Critical Role ◽  
Corneal Transplantation ◽  
Cell Loss ◽  
Corneal Dystrophy ◽  
Mitochondrial Damage ◽  
Extreme Stress ◽  
Age Related ◽  
Visual Complaints

Fuchs endothelial corneal dystrophy (FECD) is a genetically complex, heterogenous, age-related degenerative disease of corneal endothelial cells (CEnCs), occurring in the fifth decade of life with a higher incidence in females. It is characterized by extracellular matrix (ECM) protein deposition called corneal guttae, causing light glare and visual complaints in patients. Corneal transplantation is the only treatment option for FECD patients, which imposes a substantial socioeconomic burden. In FECD, CEnCs exhibit stress-induced senescence, oxidative stress, DNA damage, heightened reactive oxygen species (ROS) production, mitochondrial damage, and dysfunction as well as sustained endoplasmic reticulum (ER) stress. Among all of these, mitochondrial dysfunction involving altered mitochondrial bioenergetics and dynamics plays a critical role in FECD pathogenesis. Extreme stress initiates mitochondrial damage, leading to activation of autophagy, which involves clearance of damaged mitochondria called auto(mito)phagy. In this review, we discuss the role of mitochondrial dysfunction and mitophagy in FECD. This will provide insights into a novel mechanism of mitophagy in post-mitotic ocular cell loss and help us explore the potential treatment options for FECD.

scholarly journals Mitochondria and Parkinson’s Disease: Clinical, Molecular, and Translational Aspects

2020 ◽  
pp. 1-16 ◽  
Author(s):  
Max Borsche ◽  
Sandro L. Pereira ◽  
Christine Klein ◽  
Anne Grünewald
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Mitochondrial Dysfunction ◽  
Autosomal Dominant ◽  
Alpha Synuclein ◽  
Therapeutic Approaches ◽  
Polymerase Gamma ◽  
Mitochondrial Toxins ◽  
Molecular Patterns ◽  
Damage Associated Molecular Patterns

Mitochondrial dysfunction represents a well-established player in the pathogenesis of both monogenic and idiopathic Parkinson’s disease (PD). Initially originating from the observation that mitochondrial toxins cause PD, findings from genetic PD supported a contribution of mitochondrial dysfunction to the disease. Here, proteins encoded by the autosomal recessively inherited PD genes Parkin, PTEN-induced kinase 1 (PINK1), and DJ-1 are involved in mitochondrial pathways. Additional evidence for mitochondrial dysfunction stems from models of autosomal-dominant PD due to mutations in alpha-synuclein (SNCA) and leucine-rich repeat kinase 2 (LRRK2). Moreover, patients harboring alterations in mitochondrial polymerase gamma (POLG) often exhibit signs of parkinsonism. While some molecular studies suggest that mitochondrial dysfunction is a primary event in PD, others speculate that it is the result of impaired mitochondrial clearance. Most recent research even implicated damage-associated molecular patterns released from non-degraded mitochondria in neuroinflammatory processes in PD. Here, we summarize the manifold literature dealing with mitochondria in the context of PD. Moreover, in light of recent advances in the field of personalized medicine, patient stratification according to the degree of mitochondrial impairment followed by mitochondrial enhancement therapy may hold potential for at least a subset of genetic and idiopathic PD cases. Thus, in the second part of this review, we discuss therapeutic approaches targeting mitochondrial dysfunction with the aim to prevent or delay neurodegeneration in PD.

Abstract 247: Mitochondrial Damage Associated Molecular Patterns Promotes Endothelial Dysfunction in the Microcirculation

2018 ◽  
Vol 123 (Suppl_1) ◽  
Author(s):  
Karima Ait-Aissa ◽  
Andrew O Kadlec ◽  
Dawid S Chabowski ◽  
Joseph C Hockenberry ◽  
Jasmine M Linn ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Mitochondrial Damage ◽  
Molecular Patterns ◽  
Damage Associated Molecular Patterns

scholarly journals Mitochondrial damage-associated molecular patterns released by abdominal trauma suppress pulmonary immune responses

2014 ◽  
Vol 76 (5) ◽  
pp. 1222-1227 ◽  
Author(s):  
Cong Zhao ◽  
Kiyoshi Itagaki ◽  
Alok Gupta ◽  
Stephen Odom ◽  
Nicola Sandler ◽  
...  
Keyword(s):  
Immune Responses ◽  
Abdominal Trauma ◽  
Mitochondrial Damage ◽  
Molecular Patterns ◽  
Damage Associated Molecular Patterns

Mangiferin improves hepatic damage-associated molecular patterns, lipid metabolic disorder and mitochondrial dysfunction in alcohol hepatitis rats

2019 ◽  
Vol 10 (6) ◽  
pp. 3514-3534 ◽  
Author(s):  
Mengran Li ◽  
Chunxiao Wu ◽  
Hongbin Guo ◽  
Ce Chu ◽  
Mingye Hu ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Metabolic Network ◽  
Metabolic Disorder ◽  
Hepatic Damage ◽  
Molecular Patterns ◽  
Damage Associated Molecular Patterns ◽  
Lipid Metabolic Disorder ◽  
Alcohol Hepatitis

Mangiferin ameliorated the progression of AH by regulating the metabolic network associated with damage-associated molecular patterns, lipid metabolic disorder and mitochondrial dysfunction in AH rats.

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