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April 18, 2026Communications Biology0 citationsOpen Access

Lipid homeostasis plays a critical role in inherited and acquired retinal diseases

ABAnwesha BhattacharyyaVCVineet Choudhary

Key Points

  • This review aims to explore the crucial role of lipid homeostasis in retinal function and disease pathology.
  • Review of existing literature on lipid homeostasis and retinal diseases.
  • Analysis of mechanisms linking lipid dysregulation to retinal pathologies.
  • Summary of strategies to address the consequences of dysregulated lipids.
  • Dysregulated lipid homeostasis leads to oxidative stress and mitochondrial dysfunction.
  • Impaired signal transduction contributes to retinal degeneration.
  • Various acquired and genetic factors disrupt normal lipid balance, affecting retinal health.

Abstract

The photoreceptor layer of the retina converts light stimuli into electrical signals and transmits them to the visual cortex for image processing. Photoreceptor cells rely on a constant supply of nutrients, including lipids, to replenish their high demand of membrane remodelling. Dysregulated retinal lipid homeostasis results in ectopic lipid deposition that triggers oxidative stress, inflammatory response, mitochondrial dysfunction, and impaired signal transduction, thereby contributing to the pathogenesis of retinal degeneration in several eye diseases. In this review, we discuss the importance of lipid homeostasis in the normal functioning of the retina and how dysregulation in this process due to genetic or acquired factors manifests in various retinal pathologies. We summarize potential strategies to mitigate the pathological effects of retinal diseases. A review summarizes the importance of lipid homeostasis in the normal functioning of the retina and how dysregulation in this process due to genetic or acquired factors manifests in various retinal pathologies.

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Cite This Study

Bhattacharyya et al. (2026) studied this question.

synapsesocial.com/papers/69e31ff140886becb653f1bdhttps://doi.org/10.1038/s42003-026-10025-1
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