Mechanistic Insights of Retinal Diseases and Directions for New Therapeutics

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: 31 August 2026 | Viewed by 1133

Editors

Department of Ophthalmology, Boston Children’s Hospital, Harvard Medical School, Boston, MA 02115, USA
Interests: retinopathy; age-related macular degeneration; angiogenesis; blood–retinal barrier; inflammation; retinal pigment epithelium; Wnt signaling; nuclear receptors
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Guest Editor
Department of Ophthalmology, Boston Children’s Hospital, Harvard Medical School, Boston, MA 02115, USA
Interests: age-related macular degeneration; neuroinflammation; neurodegeneration; retinal degeneration; Alzheimer’s disease

Special Issue Information

Dear Colleagues,

Retinal diseases are major global health burdens and the leading cause of vision loss worldwide, yet effective therapies remain limited for many conditions. These include age-related macular degeneration, diabetic retinopathy, glaucoma, and inherited retinal degeneration. Progress in the development of new therapeutics depends on mechanistic insights into disease pathogenesis and research on cellular and molecular basis of retinal metabolic homeostasis, neurovascular interaction, and ocular immune responses that are often dysregulated during retinal disease processes. Signaling pathways involving cellular lipid and glucose metabolism, oxidative stress, inflammation, complement, and neuronal protection are central to the pathogenesis of major retinal disorders. Translating these mechanistic insights into clinically effective treatments remains a critical challenge. In this Special Issue, we aim to encompass fundamental research in preclinical models of eye diseases and provide new directions towards potential therapeutics for clinical applications. By integrating mechanistic insights with emerging therapeutic perspectives, this Special Issue seeks to advance our understanding of the pathogenesis of retinal diseases and promote the development of more effective and targeted mechanism-based therapies to ultimately prevent vision loss in children and adults.

Dr. Jing Chen
Dr. Neetu Kushwah
Guest Editors

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Keywords

  • retinopathy
  • AMD
  • retinal degeneration
  • ocular pharmacology
  • translational therapeutics

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Published Papers (1 paper)

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Review

18 pages, 1746 KB  
Review
Immunometabolic Regulation of Neuroinflammation in Retinitis Pigmentosa: Roles of Microglia, Müller Glia, and Regulated Cell Death
by Yijing Yang, Pai Zhou, Ying Deng and Qinghua Peng
Biomolecules 2026, 16(3), 364; https://doi.org/10.3390/biom16030364 - 28 Feb 2026
Viewed by 864
Abstract
Chronic neuroinflammation is increasingly implicated in the progression of neurodegenerative diseases, yet the mechanisms linking metabolic stress, innate immune activation, and neuronal vulnerability remain incompletely defined. Retinitis pigmentosa (RP), despite its genetic heterogeneity, exhibits convergent inflammatory and metabolic alterations during disease progression, providing [...] Read more.
Chronic neuroinflammation is increasingly implicated in the progression of neurodegenerative diseases, yet the mechanisms linking metabolic stress, innate immune activation, and neuronal vulnerability remain incompletely defined. Retinitis pigmentosa (RP), despite its genetic heterogeneity, exhibits convergent inflammatory and metabolic alterations during disease progression, providing a useful model for studying immune-mediated neurodegeneration. This review summarizes current evidence from experimental models of retinal degeneration and human retinal studies to examine how sustained neuroinflammation is established in RP. We focus on the coordinated roles of retinal microglia and Müller glia in sensing photoreceptor stress and shaping the inflammatory microenvironment. Microglia are activated early in disease and contribute to progression through inflammatory signaling, phagoptosis, metabolic adaptation, and inflammasome-associated pathways. Müller glia, in turn, modulate metabolic homeostasis and propagate inflammatory signals across retinal layers. We also discuss how stress-responsive regulatory pathways, including p53-associated signaling, influence redox balance, iron handling, and inflammatory persistence without acting as primary apoptotic drivers. Together, these findings support a model in which chronic immunometabolic dysregulation contributes to retinal degeneration and highlight inflammation-related processes as potential targets for mutation-independent therapeutic strategies. Full article
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