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Abstract
Diabetic patients suffer from a host of physiological abnormalities beyond just those of glucose metabolism. These abnormalities often lead to systemic inflammation via modulation of several inflammation-related genes, their respective gene products, homocysteine metabolism, and pyroptosis. The very nature of this homeostatic disruption re-sets the overall physiology of diabetics via upregulation of immune responses, enhanced retinal neovascularization, upregulation of epigenetic events, and disturbances in cells’ redox regulatory system. This altered pathophysiological milieu can lead to the development of diabetic retinopathy (DR), a debilitating vision-threatening eye condition with microvascular complications. DR is the most prevalent cause of irreversible blindness in the working-age adults throughout the world as it can lead to severe structural and functional remodeling of the retina, decreasing vision and thus diminishing the quality of life. In this manuscript, we attempt to summarize recent developments and new insights to explore the very nature of this intertwined crosstalk between components of the immune system and their metabolic orchestrations to elucidate the pathophysiology of DR. Understanding the multifaceted nature of the cellular and molecular factors that are involved in DR could reveal new targets for effective diagnostics, therapeutics, prognostics, preventive tools, and finally strategies to combat the development and progression of DR in susceptible subjects.
Highlights
Despite advances in medical health and technologies, the incidence of diabetes has reached epidemic proportions globally and diabetic complications are increasing throughout the world, e.g., diabetic retinopathy (DR)
We demonstrated that Hcy could potentially mediate the expression of inflammatory markers in human retinal cells without interfering with their cellular morphologies or their genomic integrities (Singh and Tyagi, 2017a)
The principal mode of actions of the drugs rely upon the observations that up to 90% of the glucose is filtered by the kidney is absorbed back by a low-affinity/high-capacity sodium-glucose co-transporter 2 (SGLT2) that is expressed in the S1 and S2 segments of the proximal tubule in the kidneys
Summary
Despite advances in medical health and technologies, the incidence of diabetes has reached epidemic proportions globally and diabetic complications are increasing throughout the world, e.g., DR. VEGF is made by many types of retinal cells, including RPE, Muller, ganglion, glial, and endothelial cells (Huang et al, 2011; Sun et al, 2012) and it has been studied extensively It is considered a critical factor related to the BRB breakdown and its levels have been found to be significantly higher in DME patients than non-diabetics ones (Funatsu et al, 2002; Caldwell et al, 2003). Many types of epigenetic regulations, such as histone post-translational modifications in chromatin or DNA methylation, and the involvement of specific signature(s) governed by various RNA species have been associated with DR Such discoveries point to the fact that the new field of “epigenomics” and its implications in DR and related pathologies are continually evolving such as the expression of pathological genes was found to be altered in endothelial and vascular smooth muscle cells without inducing any changes in the underlying DNA sequences of these cells (Figure 3). Ruboxistaurin (PKC β inhibitor) downregulates ADM expression and activity, and electroretinography (ERG) showed that this change helped preserve the retinal functions suggesting that ADM/NO pathway could serve as a potential therapeutic target for DR (Midena and Pilotto, 2017)
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