Sahajpal Nikhil Shri, Goel Rajesh Kumar, Chaubey Alka, Aurora Rohan, Jain Subheet Kumar
Department of Pharmaceutical Sciences, Guru Nanak Dev University, Amritsar, Punjab, India.
Department of Pharmaceutical Sciences and Drug Research, Punjabi University, Patiala, India.
Curr Protein Pept Sci. 2019;20(1):92-110. doi: 10.2174/1389203719666180928123449.
Diabetic retinopathy (DR) remains the leading cause of blindness in working-aged adults around the world. The proliferative diabetic retinopathy (PDR) and diabetic macular edema (DME) are the severe vision threatening stages of the disorder. Although, a huge body of research exists in elaborating the pathological mechanisms that lead to the development of DR, the certainty and the correlation amongst these pathways remain ambiguous. The complexity of DR lies in the multifactorial pathological perturbations that are instrumental in both the disease development and its progression. Therefore, a holistic perspective with an understanding of these pathways and their correlation may explain the pathogenesis of DR as a unifying mechanism. Hyperglycemia, oxidative stress and inflammatory pathways are the crucial components that are implicated in the pathogenesis of DR. Of these, hyperglycemia appears to be the initiating central component around which other pathological processes operate. Thus, this review discusses the role of hyperglycemia, oxidative stress and inflammation in the pathogenesis of DR, and highlights the cross-talk amongst these pathways in an attempt to understand the complex interplay of these mechanisms. Further, an effort has been made to identify the knowledge gap and the key players in each pathway that may serve as potential therapeutic drug targets.
糖尿病性视网膜病变（DR）仍是全球劳动年龄成年人失明的主要原因。增殖性糖尿病性视网膜病变（PDR）和糖尿病性黄斑水肿（DME）是该疾病严重威胁视力的阶段。尽管在阐述导致DR发生的病理机制方面已有大量研究，但这些途径之间的确定性和相关性仍不明确。DR的复杂性在于多因素病理扰动，这些扰动在疾病的发生和发展中都起作用。因此，从整体角度理解这些途径及其相关性，可能会将DR的发病机制解释为一种统一机制。高血糖、氧化应激和炎症途径是DR发病机制中的关键组成部分。其中，高血糖似乎是引发其他病理过程围绕其运作的核心起始成分。因此，本综述讨论了高血糖、氧化应激和炎症在DR发病机制中的作用，并强调了这些途径之间的相互作用，试图理解这些机制的复杂相互作用。此外，还努力确定了各途径中的知识空白和关键参与者，这些可能成为潜在的治疗药物靶点。
