The primary role of meibomian glands (MGs) is to actively synthesize and secret lipids and proteins spread onto the tear film, and the glandular lipids promote tear stability, prevent evaporation, and reduce friction. Meibomian gland dysfunction (MGD) is the leading cause of dry eye disease and one of the most common ophthalmic problems worldwide. MGs are densely innervated and regulated by hormones and growth factors. However, since the polar and nonpolar lipids are produced through processes in MGs that are not completely understood, a relevant question has been raised: Would the altered systemic lipids metabolism affect the physiology and structure of MGs? This review introduces the recent update regarding the relationships between serum lipid and MGD in clinical and basic research while providing answers to this question. A causal relationship remains to be established; however, serum lipid level or dyslipidemia may be related to MGD directly or indirectly, or both. Further studies are warranted to establish the role of serum lipid level and meibocyte differentiation/maturation and lipid synthesis.
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http://dx.doi.org/10.3390/jcm11144010 | DOI Listing |
J Complement Integr Med
January 2025
Department of Basic Medical Sciences, Manipal, Manipal Academy of Higher Education, Manipal, Karnataka, India.
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Department of Pharmacology and Toxicology, Faculty of Pharmacy in Hradec Králové, Charles University, Hradec Králové, Czech Republic.
Familial hypercholesterolemia (FH) is a relatively rare genetic disease associated with high serum cholesterol levels but also with abnormalities in blood coagulation. Novel pharmacotherapeutic approaches in FH including proprotein convertase subtilisin/kexin type 9 antibodies (PCSK9Ab) are very efficient in decreasing cholesterol levels but their impact on coagulation in FH is not yet established. Therefore, we hypothesized that these novel antidyslipidemic drugs can positively impact blood coagulation due to their more potent effect on cholesterol.
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Isakson Center for Neurological Disease Research, College of Veterinary Medicine, University of Georgia, Athens, GA, USA.
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December 2024
University of Southern California, Los Angeles, CA, USA.
Background: APOE4 carriers exhibit cerebrovascular dysfunction which may contribute to the development of cognitive decline and dementia; however, the mechanisms underlying this pathophysiology remain unknown. Impaired cerebrovascular reactivity (CVR) may be associated with vascular injury, inflammation, and endothelial dysfunction. To examine whether these processes may be involved in CVR deficits in APOE4 carriers, we explored whether plasma levels of vascular injury markers indicative of inflammation and endothelial dysfunction are associated with impaired CVR to hypercapnia and hypocapnia in older APOE4 carriers.
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University of Kansas Alzheimer's Disease Research Center, Fairway, KS, USA.
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