Matrix metalloproteinases in keratoconus – Too much of a good thing?

Martino, Erica di; Ali, Manir; Inglehearn, Chris F.

doi:10.1016/j.exer.2019.03.016

Cited by 56 publications

(48 citation statements)

References 88 publications

(101 reference statements)

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“…The main factor may be matrix metalloproteinases. 23 Higher matrix metalloproteinase levels in the tear fluid of developing or progressive keratoconus may change the corneal structure. It is stimulated by inflammation and some hormones influence inflammation.…”

Section: Discussionmentioning

confidence: 99%

Association Between Keratoconus and Thyroid Gland Dysfunction: A Cross-Sectional Case–Control Study

Elmassry¹,

Doheim²,

Iqbal³

et al. 2020

J Refract Surg

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K eratoconus is a corneal ectatic disorder that starts at puberty and decreases the radius of curvature of the central cornea. 1 Kennedy et al. 2 reported that the incidence rate is 1 per 50,000 among the population. Moreover, the pathophysiological processes underlying keratoconus have not been fully explained and proposed mechanisms including oxidative dam-age, proteolytic degradation in the corneal stroma, epithelial mechanical injury, immunological factors, and genetic factors have been suggested. [1][2][3][4] reported an incidence of keratoconus in 3.5% to 8% of patients with Down syndrome. Furthermore, hormonal imbalances affect the corneal metabolism and may be associated with keratoconus. Likewise, thyroid gland ABSTRACT PURPOSE: To examine the clinical association between thyroid gland dysfunction and keratoconus. METHODS:This was a cross-sectional case-control study conducted between May 2018 and July 2019. After performing Pentacam (Oculus Optikgeräte GmbH, Wetzlar, Germany) examination, flat, steep, and maximum simulated keratometric readings were recorded for each patient. Serum concentrations of free triiodothyronine, free thyroxine, and thyroidstimulating hormone were measured. Further examinations by an endocrinologist were indicated for patients with positive laboratory results to confirm thyroid gland dysfunction. RESULTS:One hundred eighty-seven patients with bilateral keratoconus and 187 sex-and age-matched healthy controls without keratoconus were analyzed. Mean age was 26.4 ± 8.2 years for the patients with keratoconus and 27.1 ± 9.4 years for the control patients, with no significant difference. The results showed that thyroid gland dysfunction prevalence was 10 of 187 patients with keratoconus (5.3%) and 2 of 187 control patients (1.1%), and the difference was statistically significant (P = .036). For the patients with keratoconus and thyroid gland dysfunction, 8 were women and 2 were men. Additionally, 6 patients (2 men and 4 women) had hyperthyrosis and 4 women had hypothyrosis. For controls, the two patients had hypothyrosis. CONCLUSIONS:This study showed that there is a possible association between keratoconus and thyroid gland dysfunction, but more studies are needed to build upon these results.[J Refract Surg. 2020;36(4):253-257.] (AT). © 2020 El-Massry, Doheim, Iqbal, et al.; licensee SLACK Incorporated. This is an Open Access article distributed under the terms of the Creative Commons . This license allows users to copy and distribute, to remix, transform, and build upon the article non-commercially, provided the author is attributed and the new work is non-commercial.

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Section: Discussionmentioning

confidence: 99%

Association Between Keratoconus and Thyroid Gland Dysfunction: A Cross-Sectional Case–Control Study

Elmassry¹,

Doheim²,

Iqbal³

et al. 2020

J Refract Surg

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“…Interaction analysis by RT‐PCR and Western blot illustrated that MMP2 protein level was negatively correlated with miR‐214‐3p, which was positively correlated with PVT1. The modulators matrix metalloproteinases (MMPs) family plays critical roles in the TGFβ2‐mediated matrix contraction . Besides, MMP2 is closely correlated with the proliferation of lens epithelial cells.…”

Section: Discussionmentioning

confidence: 99%

“…The modulators matrix metalloproteinases (MMPs) family plays critical roles in the TGFβ2-mediated matrix contraction. [26][27][28] Besides, MMP2 is closely correlated with the proliferation of lens epithelial cells. Therefore, lncRNA PVT1 could regulate the HLE B-3 cell biological activity via modulating the MMP2.…”

Section: Discussionmentioning

confidence: 99%

SP1‐mediated lncRNA PVT1 modulates the proliferation and apoptosis of lens epithelial cells in diabetic cataract via miR‐214‐3p/MMP2 axis

Yang

Tian

2019

J Cellular Molecular Medi

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Emerging evidence illustrates the critical roles of long non‐coding RNAs (lncRNAs) in the diabetes. However, the deepgoing regulation of lncRNA PVT1 in the diabetic cataract (DC) is still unclear. Here, present research investigates the pathologic roles and underlying mechanism by which lncRNA PVT1 regulates the DC pathogenesis. Human lens epithelial (HLE) B‐3 cells were induced by the high glucose (HG) to simulate the DC microenvironment models. Results revealed that lncRNA PVT1 expression was up‐regulated in the HG‐induced HLE B‐3 cells as compared to the normal glucose group. Transcription factor SP1 could bind with the promoter region of PVT1 and activate its transcription. Functionally, PVT1 knock‐down could repress the proliferation and promote the apoptosis of HLE B‐3 cells. Mechanistically, PVT1 acted as the ‘miRNA sponge’ to target miR‐214‐3p/MMP2 axis. This finding revealed a novel insight of lncRNA PVT1 for the DC pathogenesis, providing an inspiration for the DC mechanism.

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“…Inconsistent findings are also reported for MMP-3, MMP-7 and MMP-13 [128]. All in all, there are consistent evidence on elevated MMP-9 levels in keratoconus cornea tissues and tears.…”

Section: Matrix Metalloproteinasesmentioning

confidence: 61%

“…MMP-1 and MMP-9, are upregulated in corneal tissue and affect collagen properites and dyregulate proteolysis [128]. In a pathways enrichment analysis of 19 keratoconus genes consistently reported as risk genes to keratoconus in 16 studies, interleukin-1 processing and assembly of collagen fibrils are associated with keratoconus pathology [129].…”

Section: Matrix Metalloproteinasesmentioning

confidence: 99%

Molecular Genetics of Keratoconus: Clinical Implications

Wang¹,

Pang²

2021

Ocular Surface Diseases - Some Current Date on Tear Film Problem and Keratoconic Diagnosis

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Occurrence of keratoconus is pan-ethnic with reported prevalence ranging widely from 1:400 to about 1:8000, higher in Asian than Western populations. Its genetics is complex with undefined pattern of inheritance. Familial traits are also known. More than 50 gene loci and 200 variants are associated with keratoconus, some through association studies with quantitative traits of cornea features including curvature and central thickness. Environmental, behavioral, and epigenetic factors are also involved in the etiology, likely interactively with genetic susceptibility. Regardless of sex and age of disease onset, clinical courses and responses to treatment vary. Keratoconus is a major cause of cornea transplantation and is potentially blinding. Currently collagen cross-linking provides effective treatment although responses from some patients can be unpredictable with complications. Early diagnosis is vital to obtain good treatment outcome, but in many patients early signs and symptoms are not obvious. While there are potential biomarkers, reliable presymptomatic detection and prediction of treatment response may require multitude of gene variants, cornea properties, and external risk factors.

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Matrix metalloproteinases in keratoconus – Too much of a good thing?

Abstract: This is a repository copy of Matrix metalloproteinases in keratoconus-too much of a good thing?.

Cited by 56 publications

References 88 publications

Association Between Keratoconus and Thyroid Gland Dysfunction: A Cross-Sectional Case–Control Study

Association Between Keratoconus and Thyroid Gland Dysfunction: A Cross-Sectional Case–Control Study

SP1‐mediated lncRNA PVT1 modulates the proliferation and apoptosis of lens epithelial cells in diabetic cataract via miR‐214‐3p/MMP2 axis

Molecular Genetics of Keratoconus: Clinical Implications

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