ArticleAmerican journal of physiology. Renal physiology2019
Stress granules are formed in renal proximal tubular cells during metabolic stress and ischemic injury for cell survival.
Article in American journal of physiology. Renal physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 20 citations in OpenAlex.
- Loss of O-GlcNAc transferase activity impairs the dynamic formation of protective stress granules in ischemic cardiomyocytes.The Biochemical journal · 2026Article
- PAX gene expression in autosomal dominant polycystic kidney disease contributes to cyst expansion and regulates a gene network associated with cyst growth.Human molecular genetics · 2026Article
- Chronic stress disrupts the network among stress granules, P-bodies, and motor proteins.bioRxiv : the preprint server for biology · 2026Article
- The crucial role of N6-methyladenosine modification in acute kidney injury: mechanisms and therapeutic potential.Frontiers in immunology · 2026Review
- Connecting the Dots: Stress Granule and Cardiovascular Diseases.Journal of cardiovascular translational research · 2025Review
- Review
- Pseudogene GSTM3P1 derived long non-coding RNA promotes ischemic acute kidney injury by target directed microRNA degradation of kidney-protective mir-668.Kidney international · 2024Article
- Protective and Adverse Roles of DDX3X in Different Cell Types in Nonalcoholic Steatohepatitis Progression.Research (Washington, D.C.) · 2023Article
- O-GlcNAcylation in Renal (Patho)Physiology.International journal of molecular sciences · 2022Review
- An optimized protocol for single nuclei isolation from clinical biopsies for RNA-seq.Scientific reports · 2022Article
- Mitochondrial Inhibition by Sodium Azide Induces Assembly of eIF2α Phosphorylation-Independent Stress Granules in Mammalian Cells.International journal of molecular sciences · 2022Article
- RNA-binding proteins and their role in kidney disease.Nature reviews. Nephrology · 2022Review
- The enigma of ultraviolet radiation stress granules: Research challenges and new perspectives.Frontiers in molecular biosciences · 2022Article
- Stress Granules in the Anti-Cancer Medications Mechanism of Action: A Systematic Scoping Review.Frontiers in oncology · 2021Article
- Revisiting the Concept of Stress in the Prognosis of Solid Tumors: A Role for Stress Granules Proteins?Cancers · 2020Review
- Understanding the roles of stress granule during chemotherapy for patients with malignant tumors.American journal of cancer research · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Stress granules (SGs) are a type of cytoplasmic structures formed in eukaryotic cells upon cell stress, which mainly contain RNA-binding proteins and RNAs. The formation of SGs is generally regarded as a mechanism for cells to survive a harsh insult. However, little is known about SG formation and function in kidneys. To address this, we applied different kinds of stressors to cultured proximal tubular cells as well as a short period of ischemia-reperfusion to mouse kidneys. It was found that glycolytic inhibitors such as 2-deoxy-d-glucose and 3-(3-pyridinyl)-1-(4-pyridinyl)-2-propen-1-one induced SG formation within 30 min in these cells. Similarly, SGs were induced by inhibitors of mitochondrial respiration such as sodium azide and CCCP. Renal ischemia-reperfusion induced SG formation in the cells of proximal tubules. To test the role of SGs, we stably knocked down G3bp1, a SG core protein, in renal tubular cells by shRNA viral transduction. As expected, knockdown of G3bp1 largely disrupted the assembly of SGs. After azide or cisplatin treatment, more dead cells were found in knockdown cells compared with controls, accompanied by increases in cleaved/active caspase-3. Reintroduction of exogenous G3bp1 into knockdown cells could rescue the cell death phenotype. Taken together, our data provide the first evidence of SG formation in renal tubular cells during metabolic stress and acute kidney injury. SGs are formed to protect proximal tubular cells under these conditions. Modulation of SG biogenesis may provide a novel approach to lessen the severity of renal diseases.
Indexed as
Identifiers
What OpenQuestion holds
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.