ABSTRACT
A serious consequence of diabetes mellitus, diabetic nephropathy (DN) which causes gradual damage to the kidneys. Dietary changes, blood pressure control, glucose control, and hyperlipidemia are all important components of DN management. New research, however, points to microRNAs (miRNAs) as having a pivotal role in DN pathogenesis. Miniature non-coding RNA molecules such as miRNAs control gene expression and impact several biological processes. The canonical and non-canonical routes of miRNA biogenesis are discussed in this article. In addition, several important signaling pathways are examined in the study of miRNA regulation in DN. A deeper knowledge of these regulatory mechanisms would allow for a better understanding of the molecular basis of DN and the development of innovative therapeutic strategies. Finally, miRNAs show tremendous potential as DN diagnostic biomarkers and treatment targets, opening up promising avenues for further study and potential clinical use.
Subject(s)
Diabetes Mellitus , Diabetic Nephropathies , MicroRNAs , Humans , MicroRNAs/genetics , MicroRNAs/metabolism , Diabetic Nephropathies/metabolism , Kidney/metabolism , Signal Transduction/geneticsABSTRACT
Pancreatic cancer (PC) is one of the deadliest cancers associated with poor prognosis. The lack of reliable means of early cancer detection contributes to this disease's dismal prognosis. Long non-coding RNAs (LncRNAs) are protein-free RNAs produced by genome transcription; they play critical roles in gene expression regulation, epigenetic modification, cell proliferation, differentiation, and reproduction. Recent research has shown that lncRNAs play important regulatory roles in PC behaviors, in addition to their recently found functions. Several in-depth investigations have shown that lncRNAs are strongly linked to PC development and progression. Here, we discuss how lncRNAs, which are often overlooked, play many roles as regulators in the molecular mechanism underlying PC. This review also discusses the involved LncRNAs in PC pathogenesis and treatment resistance.