ReviewPediatric nephrology (Berlin, Germany)2019
Endoplasmic reticulum stress and monogenic kidney diseases in precision nephrology.
Review in Pediatric nephrology (Berlin, Germany), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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.
The trial behind it
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
25 citing papers in PubMed, 61 citations in OpenAlex.
- Construction, evaluation, and applications of renal barrier-on-a-chip system.Bioactive materials · 2026Review
- Pathogenic mechanisms in Fabry disease.Frontiers in medicine · 2026Review
- Podocyte injury damages podocytes in chimeric organoids.PloS one · 2026Article
- Genotype-Based Molecular Mechanisms in Alport Syndrome.Journal of the American Society of Nephrology : JASN · 2025Review
- Endoplasmic reticulum stress as a driver and therapeutic target for kidney disease.Nature reviews. Nephrology · 2025Review
- Misprocessing of α -Galactosidase A, Endoplasmic Reticulum Stress, and the Unfolded Protein Response.Journal of the American Society of Nephrology : JASN · 2025Article
- Therapeutic implications of endoplasmic reticulum stress gene CCL3 in cervical squamous cell carcinoma.Cell biology and toxicology · 2025Article
- Case-inspired exploration of renin mutations in autosomal dominant tubulointerstitial kidney disease: not all paths lead to the endoplasmic reticulum.Pediatric nephrology (Berlin, Germany) · 2024Article
- The double whammy of ER-retention and dominant-negative effects in numerous autosomal dominant diseases: significance in disease mechanisms and therapy.Journal of biomedical science · 2024Review
- Research progress on endoplasmic reticulum homeostasis in kidney diseases.Cell death & disease · 2023Review
- Targeting Endoplasmic Reticulum for Novel Therapeutics and Monitoring in Acute Kidney Injury.Nephron · 2023Review
- CRELD2, endoplasmic reticulum stress, and human diseases.Frontiers in endocrinology · 2023Review
- Endoplasmic reticulum stress increases exosome biogenesis and packaging relevant to sperm maturation in response to oxidative stress in obese mice.Reproductive biology and endocrinology : RB&E · 2022Article
- Endoplasmic-reticulum-stress-induced lipotoxicity in human kidney epithelial cells.Toxicology research · 2022Article
- Hydrogen Sulfide Plays an Important Role by Regulating Endoplasmic Reticulum Stress in Diabetes-Related Diseases.International journal of molecular sciences · 2022Review
- More dissimilarities than affinities between DNAJB11-PKD and ADPKD.Clinical kidney journal · 2022Article
- Upregulation of C/EBP Homologous Protein induced by ER Stress Mediates Epithelial to Myofibroblast Transformation in ADTKD-UMOD.International journal of medical sciences · 2022Article
- Intrarenal Single-Cell Sequencing of Hepatitis B Virus Associated Membranous Nephropathy.Frontiers in medicine · 2022Article
- Role of PKD2 in the endoplasmic reticulum calcium homeostasis.Frontiers in physiology · 2022Review
- Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The advent of next-generation sequencing (NGS) in recent years has led to a rapid discovery of novel or rare genetic variants in human kidney cell genes, which is transforming the risk assessment, diagnosis, and treatment of kidney disease. Mutations may lead to protein misfolding, disruption of protein trafficking, and endoplasmic reticulum (ER) retention. An imbalance between the load of misfolded proteins and the folding capacity of the ER causes ER stress and unfolded protein response. Mutations in nephrin (NPHS1), podocin (NPHS2), laminin β2 (LAMB2), and α-actinin-4 (ACTN4) have been shown to induce ER stress in HEK293 cells and podocytes in hereditary nephrotic syndromes; various founder mutations in collagen IV α chains (COL4A) have been demonstrated to activate podocyte ER stress in collagen IV nephropathies; and mutations in uromodulin (UMOD) have been reported to trigger tubular ER stress in autosomal dominant tubulointerstitial kidney disease. Meanwhile, ER resident protein SEC63 may modify disease severity in autosomal dominant polycystic kidney disease. These findings underscore the importance of ER stress in the pathogenesis of monogenic kidney disease. Recently, we have identified mesencephalic astrocyte-derived neurotrophic factor (MANF) and cysteine-rich with EGF-like domains 2 (CRELD2) as urinary ER stress biomarkers in ER stress-mediated kidney diseases.
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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.