> Publications > Minocycline prevents photoreceptor degeneration in Retinitis pigmentosa through modulating mitochondrial homeostasis

OptoDrum

Publication

February 23, 2026 • ✎ STRIA TECH

Minocycline prevents photoreceptor degeneration in Retinitis pigmentosa through modulating mitochondrial homeostasis

Topics:

Blindness

Neuroinflammation

Retinal Degeneration

Retinal Degeneration and Inherited Retinal Disease

Retinal Dystrophy

Publication

International Immunopharmacology (Sep 30, 2024) Minocycline prevents photoreceptor degeneration in Retinitis pigmentosa through modulating mitochondrial homeostasis

Shi Y, Chen Y, Pan Y, Chen G, Xiao Z, Chen X, Wang M, Liang D

DOI: 10.1016/j.intimp.2024.112703 >>

Minocyclin is a commonly used antibiotic, that also has anti-inflammatory and antioxidant properties that may benefit neurodegenerative diseases. This study investigated its effects on retinitis pigmentosa (RP), a genetic eye disorder causing vision loss. Using a mouse model (rd1), researchers found that minocycline treatment restored both the structure and function of the retina and inhibited harmful microglial activation. The study revealed that untreated RP mice had significant mitochondrial dysfunction and increased oxidative stress in their photoreceptor cells. Minocycline prevented these abnormalities, reducing mitochondrial damage and reactive oxygen species, ultimately protecting photoreceptors from degeneration. The OptoDrum device was used in this study to assess visual function in the treated mice, demonstrating the functional improvements following minocycline therapy. These findings suggest that minocycline could be a promising approach for treating RP by maintaining mitochondrial health and reducing inflammation.

Minocycline, a broad-spectrum tetracycline antibiotic, has been shown to possess anti-inflammatory and antioxidative effects in various neurodegenerative diseases. However, its specific effects on retinitis pigmentosa (RP) have not been thoroughly investigated. Therefore, the objective of this study was to explore the potential role of minocycline in treating RP. In this investigation, we used rd1 to explore the antioxidant effect of minocycline in RP. Minocycline therapy effectively restored retinal function and structure in rd1 mice at 14 days postnatal. Additionally, minocycline inhibited the activation of microglia. Moreover, RNA sequencing analysis revealed a significant downregulation in the expression of mitochondrial genes within the retina of rd1 mice. Further KEGG and GO pathway analysis indicated impaired oxidative phosphorylation and electron transport chain processes. TEM confirmed the presence of damaged mitochondria in photoreceptors, while JC-1 staining demonstrated a decrease in mitochondrial membrane potential, accompanied by an increase in mitochondrial reactive oxygen species (ROS) levels. However, treatment with minocycline successfully reversed the abnormal expression of mitochondrial genes and reduced the levels of mitochondrial ROS, thereby providing protection against photoreceptor degeneration. Collectively, minocycline demonstrated the ability to rescue photoreceptor cells in RP by effectively modulating mitochondrial homeostasis and subsequently inflammation. These findings hold significant implications for the development of potential therapeutic strategies for RP.