ABSTRACT
Retinitis pigmentosa (RP) is the most common type of inherited retinal dystrophy. The course of RP is irreversible and leads to progressive loss of vision. It is characterized by hypotrophic degeneration of photoreceptor cells and retinal pigment epithelium. Multiple factors are involved in the development of the disease, including apoptosis, oxidative stress, and inflammatory/immune responses. In the past decades, gene therapy, stem cell therapy and other therapeutic approaches have been extensively investigated. However, due to the heritability and high heterogeneity of the disease and the difficulty in diagnosis and treatment, there is still a lack of standardized and effective therapies. Therefore, there is a need to develop new diagnostic and therapeutic approaches suitable for diseases with pathogenic mutations. With the understanding of the interaction between gene expression regulation and retinal pathology, the value of clinical applications of non-coding RNAs (ncRNAs) in retinal degeneration has gained attention. There is growing evidence that ncRNAs are widely distributed and involved in the regulation of multiple biological processes in the retina as well as processes associated with the development of RP, making them promising biomarkers for the diagnosis, treatment, and prognosis of RP. This paper reviews the crosstalk between ncRNA and RP, systematically discusses the role of ncRNAs in normal retinal cell physiology and RP pathogenesis and explores the potential of ncRNAs as therapeutic agents for clinical applications in RP.
ABSTRACT
Diabetic retinopathy (DR) is a severe microvascular complication of diabetes mellitus and a major cause of blindness in young adults. Multiple potential factors influence DR; however, the exact mechanisms are poorly understood. Advanced treatments for DR, including laser therapy, vitrectomy, and intraocular drug injections, slow the disease's progression but fail to cure or reverse visual impairment. Therefore, additional effective methods to prevent and treat DR are required. The biological clock plays a crucial role in maintaining balance in the circadian rhythm of the body. Poor lifestyle habits, such as irregular routines and high-fat diets, may disrupt central and limbic circadian rhythms. Disrupted circadian rhythms can result in altered glucose metabolism and obesity. Misaligned central and peripheral clocks lead to a disorder of the rhythm of glucose metabolism, and chronically high sugar levels lead to the development of DR. We observed a disturbance in clock function in patients with diabetes, and a misaligned clock could accelerate the development of DR. In the current study, we examine the relationship between circadian rhythm disorders, diabetes, and DR. We conclude that: 1) abnormal function of the central clock and peripheral clock leads to abnormal glucose metabolism, further causing DR and 2) diabetes causes abnormal circadian rhythms, further exacerbating DR. Thus, our study presents new insights into the prevention and treatment of DR.
Subject(s)
Chronobiology Disorders , Diabetes Mellitus , Diabetic Retinopathy , Young Adult , Humans , Diabetic Retinopathy/etiology , Chronobiology Disorders/complications , Biological Clocks , Circadian Rhythm , GlucoseABSTRACT
Diabetic retinopathy (DR) is the leakage and obstruction of retinal microvessels caused by chronic progressive diabetes that leads to a series of fundus lesions. If not treated or controlled, it will affect vision and even cause blindness. DR is caused by a variety of factors, and its pathogenesis is complex. Pericyte-related diseases are considered to be an important factor for DR in many pathogeneses, which can lead to DR development through direct or indirect mechanisms, but the specific mechanism remains unclear. Exosomes are small vesicles of 40-100 nm. Most cells can produce exosomes. They mediate intercellular communication by transporting microRNAs (miRNAs), proteins, mRNAs, DNA, or lipids to target cells. In humans, intermittent hypoxia has been reported to alter circulating excretory carriers, increase endothelial cell permeability, and promote dysfunction in vivo. Therefore, we believe that the changes in circulating exocrine secretion caused by hypoxia in DR may be involved in its progress. This article examines the possible roles of miRNAs, proteins, and DNA in DR occurrence and development and discusses their possible mechanisms and therapy. This may help to provide basic proof for the use of exocrine hormones to cure DR.