ReviewCells2023
Pathogenesis of Alkali Injury-Induced Limbal Stem Cell Deficiency: A Literature Survey of Animal Models.
Review in Cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed.
- Targeting injury-induced transglutaminase-2 activity with a cementoin-SLPI fusion protein: a novel therapeutic strategy for alkali-induced corneal injury.Journal of translational medicine · 2026Review
- Article
- Therapeutic Efficacy of Rapamycin in an Experimental Mouse Model of Corneal Alkali Burn.International journal of molecular sciences · 2026Article
- An enhanced-permeability amphiphilic nanogel loaded with sulforaphane for synergistic anti-oxidative and anti-ferroptotic therapy of corneal alkali burn.Journal of translational medicine · 2026Article
- Losartan Alleviates Chemical Burn-Induced Limbal Stem Cell Deficiency: Repurposing a Venerable Anti-Hypertension Drug.Investigative ophthalmology & visual science · 2026Article
- Human growth hormone-overexpressing adipose-derived stem cells enhance fibroblast activity and accelerate burn wound healing via ERK pathway therapeutic potential of ADSCs in burn wound repair.Regenerative therapy · 2025Article
- Transforming corneal alkali burn treatment: unveiling mechanisms and pioneering therapies from bench to bedside.Journal of translational medicine · 2025Review
- Rapamycin Mitigates Corneal Damage in a Mouse Model of Alkali Burn Injury.Bioengineering (Basel, Switzerland) · 2025Article
- A novel therapy to ameliorate nitrogen mustard-induced limbal stem cell deficiency using lipoprotein-like nanoparticles.NPJ Regenerative medicine · 2025Article
- Senescence and Stress Signaling Pathways in Corneal Cells After Nitrogen Mustard Injury.Cells · 2024Article
- Animal Models for Limbal Stem Cell Deficiency: A Critical Narrative Literature Review.Ophthalmology and therapy · 2024Review
- Squishy matters - Corneal mechanobiology in health and disease.Progress in retinal and eye research · 2024Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Limbal stem cell deficiency (LSCD) is a debilitating ocular surface disease that eventuates from a depleted or dysfunctional limbal epithelial stem cell (LESC) pool, resulting in corneal epithelial failure and blindness. The leading cause of LSCD is a chemical burn, with alkali substances being the most common inciting agents. Characteristic features of alkali-induced LSCD include corneal conjunctivalization, inflammation, neovascularization and fibrosis. Over the past decades, animal models of corneal alkali burn and alkali-induced LSCD have been instrumental in improving our understanding of the pathophysiological mechanisms responsible for disease development. Through these paradigms, important insights have been gained with regards to signaling pathways that drive inflammation, neovascularization and fibrosis, including NF-κB, ERK, p38 MAPK, JNK, STAT3, PI3K/AKT, mTOR and WNT/β-catenin cascades. Nonetheless, the molecular and cellular events that underpin re-epithelialization and those that govern long-term epithelial behavior are poorly understood. This review provides an overview of the current mechanistic insights into the pathophysiology of alkali-induced LSCD. Moreover, we highlight limitations regarding existing animal models and knowledge gaps which, if addressed, would facilitate development of more efficacious therapeutic strategies for patients with alkali-induced LSCD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.