LncRNA MALAT1's role in the development of retinopathy: A review

Long noncoding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) and retinopathy are 2 distinct yet interconnected areas of research in the field of ocular studies. MALAT1, with its diverse biological functions, has been extensively studied and demonstrated to play a role in various diseases, including ocular pathologies. Its involvement in alternative splicing regulation, transcriptional control, and the competing endogenous RNA (ceRNA) network suggests its potential implication in retinopathy. Retinopathy refers to a group of disorders that affect the retina, leading to vision impairment and, in severe cases, even blindness. These conditions include diabetic retinopathy, retinoblastoma, proliferative vitreoretinopathy, retinopathy of prematurity, and retinal neurodegeneration. The understanding of the molecular mechanisms underlying the development and progression of retinopathy, along with the potential involvement of MALAT1, can provide valuable insights for the diagnosis and treatment of this condition. Retinopathy, characterized by various manifestations and underlying mechanisms, presents a significant challenge in the field of ophthalmology. As a complex disease, its pathogenesis involves multifactorial factors, including angiogenic dysregulation, inflammatory responses, oxidative stress, and cellular signaling abnormalities. The emerging role of long noncoding RNA MALAT1 in retinopathy has attracted considerable attention. MALAT1 has been found to participate in multiple cellular processes, including alternative splicing regulation and transcriptional control. Additionally, the competing endogenous RNA (ceRNA) network involving MALAT1 indicates its potential relevance as a regulator in retinopathy. Further investigations into the specific mechanisms underlying MALAT1's involvement in retinopathy pathogenesis may provide valuable insights into the development of diagnostic and therapeutic approaches for managing retinal disorders.