ReviewOphthalmology and therapy2025
Parainflammation in the Ocular System: Considerations on the Underlying Mechanisms and Treatment of Dry Eye Disease.
Review in Ophthalmology and therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
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Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pooled it
- Optimization and formulation of cyclosporine-loaded nanostructured lipid carriers (NLCs) for the management of dry eye syndrome by using centre composite design approaches.International ophthalmology · 2026Article
- Phosphosulindac (OXT-328) restores the suppressed corneal sensitivity in rabbits with dry eye disease: therapeutic implications.Frontiers in drug delivery · 2026Article
- Dry Eye Disease and Psychiatric Disorders: Neuroimmune Mechanisms and Therapeutic Perspectives.International journal of molecular sciences · 2025Review
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionThe transition from regulated to dysregulated parainflammation is a new concept that needs to be elucidated to clarify the pathogenesis of dry eye disease (DED). This review summarizes the recent evidence about mechanisms that could lead to dysregulated parainflammation, proposing a new hypothesis to correlate this process with the progression to chronic inflammation.
methodsA group of European experts on DED participated in a roundtable to discuss the role of parainflammation in the most common ocular diseases with regard to DED. Starting from the roundtable contents, a narrative review was conducted through a PubMed search based on the main topics discussed, namely: parainflammation, dysfunctional parainflammation, tear film lipid and mucin alterations, and tear cortisol.
resultsParainflammation is involved in different ocular pathologies and is characterized by the involvement of the immune system and complement factors. In DED, continuous and persistent insults are responsible for the qualitative and quantitative alteration of the lipid and mucin components of the tear film. In addition, other contributing factors have recently been described, such as the reduction of cortisol synthesis by corneal epithelial cells. This altered condition leads to excessive macrophage activity, releasing cytokines and adhesion molecules, losing tissue homeostasis, and possibly progressing to chronic inflammation.
conclusionsLiterature evidence supports the crucial role of parainflammation and its usefulness in improving the diagnosis and treatment of DED. At the same time, further investigations are necessary to better define the transition from functional to dysfunctional parainflammation, including the role of ocular surface components other than the tear film.
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