MicroRNA-Mediated Mechanisms in Diabetic Nephropathy
Summary
Diabetic nephropathy arises from a complex interplay of hyperglycaemia-induced metabolic stress, haemodynamic alterations and pro-inflammatory signalling that culminate in glomerular and tubular injury. MicroRNAs (miRNAs) are small non-coding RNAs that fine-tune gene expression post-transcriptionally by binding to complementary sequences in target messenger RNAs. In diabetic nephropathy, dysregulated miRNA profiles contribute to oxidative stress, extracellular matrix accumulation, podocyte apoptosis and endothelial dysfunction. Key pathways modulated by miRNAs include the transforming growth factor-β cascade, renin-angiotensin system activation and nuclear factor erythroid 2-related factor 2 (NFE2L2)-dependent antioxidant responses. Altered miRNA expression within renal cells and in circulation offers both mechanistic insight into disease progression and the prospect of novel biomarkers or therapeutic targets. Experimental models have demonstrated that modulation of specific miRNAs can attenuate kidney fibrosis, restore redox balance and preserve glomerular filtration barrier integrity, underscoring the clinical potential of miRNA-based strategies in diabetic nephropathy.
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MicroRNA-Mediated Mechanisms in Diabetic Nephropathy publication trend
The graph below shows the total number of articles in microrna-mediated mechanisms in diabetic nephropathy across all publications each year (not limited to Nature Index journals).
Technical terms
MicroRNA (miRNA): Small non-coding RNA molecules (~22 nucleotides) that regulate gene expression by binding to complementary sequences in target mRNAs, leading to transcript degradation or translational repression.
Podocyte: Specialised epithelial cell in the kidney glomerulus that wraps around capillaries and contributes to the filtration barrier; podocyte loss is a hallmark of diabetic nephropathy.
Extracellular vesicle (EV): Membrane-bound particle released by cells, including exosomes, which can carry proteins, lipids and miRNAs to mediate intercellular communication.
Oxidative stress: Imbalance between the production of reactive oxygen species and antioxidant defences, leading to cellular damage.
Renal fibrosis: Excessive accumulation of extracellular matrix proteins in kidney interstitium and glomeruli, resulting in scarring and loss of function.
References
- Gallic Acid Alleviates Glucolipotoxicity-Induced Nephropathy by miR-709-NFE2L2 Pathway in db/db Mice on a High-Fat Diet. Journal of Agricultural and Food Chemistry (2024).
- Cordycepin from Cordyceps militaris ameliorates diabetic nephropathy via the miR-193b-5p/MCL-1 axis. Chinese Medicine (2023).
- Urinary Exosomal miRNA Signature in Type II Diabetic Nephropathy Patients. PLOS ONE (2016).
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