Molecular Mechanism in Retinal Diseases

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 284

Special Issue Editors

Department of Ophthalmology, Li Ka Shing Faculty of Medicine, The University of Hong Kong, Hong Kong 999077, China
Interests: cell death; retinal diseases; therapy

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Guest Editor
Faculty Of Medicine, University of Hong Kong, Hong Kong, China
Interests: viral hepatitis B; viral hepatitis C; steatosis; liver fibrosis; hepatocellular carcinoma
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Guest Editor
Department of Medicine, Queen Mary Hospital, The University of Hong Kong, Hong Kong, China
Interests: epidemiology; treatment; disease mechanisms; cell death; metabolism

Special Issue Information

Dear Colleagues,

Vision formation relies heavily on the retina; however, light-sensitive tissue damage tends to cause retinal diseases such as retinal degeneration, retinal detachment, and diabetic retinopathy. Though efforts have been made to address these problems, the therapeutic options for many retinal diseases are still limited. Therefore, better understanding of the underlying mechanisms would greatly benefit future treatment development.

Abnormal levels of cell death have been demonstrated in various retinal diseases (e.g., retinal degeneration, retinal detachment, and diabetic retinopathy), and cell death is therefore a potential therapeutic target. Mitochondria are essential organelles for the activation of apoptosis. Moreover, the involvement of mitochondria has also been demonstrated in other types of regulated cell death, including necroptosis, pyroptosis, and ferroptosis. For example, in the necroptotic process, mitochondrial respiration and the subsequent production of ROS can be initiated through the synergistic effect of RIPK3 and the pyruvate dehydrogenase complex. In addition, the mitochondrial outer membrane can also be permeabilized by the activated GSDMD (a membrane pore-formation complex) in pyroptosis. Furthermore, the mitochondrial tricarboxylic acid cycle can be augmented by glutaminolysis through cysteine deprivation in ferroptotic cell death.

Based on the essential character of the mitochondrion, the regulation of mitochondrion-associated cell death might have enormous therapeutic potential in various retinal diseases. Although the implications of mitochondrion-associated cell death have been addressed in various diseases, its role and use as a therapeutic target in retinal diseases are still poorly understood.

This Special Issue focuses on the molecular mechanisms of retinal diseases, including the contribution of mitochondrion-associated cell death to pathology. Manuscripts presenting other molecular mechanisms and therapeutic interventions and strategies for retinal diseases are also welcome.

Dr. Ming Yang
Guest Editor

Manuscript Submission Information

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Keywords

  • retinal diseases
  • regulated cell death
  • mitochondrion
  • therapeutic targets
  • pathology

Published Papers

There is no accepted submissions to this special issue at this moment.
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