ArticleJCI insight2019
Genetic deficiency or pharmacological inhibition of miR-33 protects from kidney fibrosis.
Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
42 citing papers in PubMed, 62 citations in OpenAlex.
- Shengqingjiangzhuo Capsules Alleviates Renal Fibrosis by Targeting Glomerular Endothelial Cells Exosome miR-31-5p/HO-1 to Suppress Tubular Epithelial Cells Ferroptosis.Clinical and experimental pharmacology & physiology · 2026Article
- Advances in peptide nucleic acid for targeting RNA and genomic DNA.Cell reports. Physical science · 2026Article
- Fatty acid metabolism: opportunities and challenges of traditional Chinese medicine in the treatment of renal fibrosis.Chinese medicine · 2026Review
- The multifaceted roles of microRNAs in nonalcoholic steatohepatitis: from pathogenic mechanisms to diagnostic and therapeutic opportunities.Frontiers in genetics · 2026Review
- Carbohydrate Ligand-Mediated Precise Kidney Delivery of PNA.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Enhancing diabetes treatment by targeted nucleic acid and drug delivery using cell-penetrating peptides, peptide nucleic acids, and receptor targeting.Frontiers in pharmacology · 2026Review
- MicroRNA-Mediated Regulation of Vascular Endothelium: From Pro-Inflammation to Atherosclerosis.International journal of molecular sciences · 2025Review
- Metabolism at the crossroads of inflammation and fibrosis in chronic kidney disease.Nature reviews. Nephrology · 2025Review
- Efficient and selective kidney targeting by chemically modified carbohydrate conjugates.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- miR-33 deletion in hepatocytes attenuates MASLD-MASH-HCC progression.JCI insight · 2024Article
- microRNA-33 controls hunger signaling in hypothalamic AgRP neurons.Nature communications · 2024Article
- Nanocarrier-Mediated Delivery of MicroRNAs for Fibrotic Diseases.Molecular diagnosis & therapy · 2024Review
- Aiming the magic bullet: targeted delivery of imaging and therapeutic agents to solid tumors by pHLIP peptides.Frontiers in pharmacology · 2024Review
- Metabolic reprogramming heterogeneity in chronic kidney disease.FEBS open bio · 2023Review
- Schistosome egg antigen stimulates the secretion of miR-33-carrying extracellular vesicles from macrophages to promote hepatic stellate cell activation and liver fibrosis in schistosomiasis.PLoS neglected tropical diseases · 2023Article
- Unlocking the potential of chemically modified peptide nucleic acids for RNA-based therapeutics.RNA (New York, N.Y.) · 2023Review
- Kidney fibrosis: from mechanisms to therapeutic medicines.Signal transduction and targeted therapy · 2023Review
- microRNA-33 deficiency in macrophages enhances autophagy, improves mitochondrial homeostasis, and protects against lung fibrosis.JCI insight · 2023Article
- Epigenetic modification in diabetic kidney disease.Frontiers in endocrinology · 2023Review
- pHLIP Peptides Target Acidity in Activated Macrophages.Molecular imaging and biology · 2022Article
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Authors and funding
19 authors at 6 institutions in 4 countries.
Funding
Abstract
Previous work has reported the important links between cellular bioenergetics and the development of chronic kidney disease, highlighting the potential for targeting metabolic functions to regulate disease progression. More recently, it has been shown that alterations in fatty acid oxidation (FAO) can have an important impact on the progression of kidney disease. In this work, we demonstrate that loss of miR-33, an important regulator of lipid metabolism, can partially prevent the repression of FAO in fibrotic kidneys and reduce lipid accumulation. These changes were associated with a dramatic reduction in the extent of fibrosis induced in 2 mouse models of kidney disease. These effects were not related to changes in circulating leukocytes because bone marrow transplants from miR-33-deficient animals did not have a similar impact on disease progression. Most important, targeted delivery of miR-33 peptide nucleic acid inhibitors to the kidney and other acidic microenvironments was accomplished using pH low insertion peptides as a carrier. This was effective at both increasing the expression of factors involved in FAO and reducing the development of fibrosis. Together, these findings suggest that miR-33 may be an attractive therapeutic target for the treatment of chronic kidney disease.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.