ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2022
SARS-CoV-2 N Protein Induces Acute Kidney Injury via Smad3-Dependent G1 Cell Cycle Arrest Mechanism.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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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
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Who cites it
56 citing papers in PubMed, 86 citations in OpenAlex.
- Single-cell Stereo-seq reveals regulatory mechanisms driving regeneration of injured proximal tubules during AKI.Nature communications · 2026Article
- Pediatric viral myocarditis: mechanisms, experimental models, and research gaps.Pediatric research · 2026Review
- Targeting coronaviral inflammation: aptamer-based strategies for emerging threats.Signal transduction and targeted therapy · 2026Article
- Annexin A13 Protects Against Acute Kidney Injury by Inactivating TGF-β/Smad3 Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Identification and mechanism analysis of biomarkers related to butyrate metabolism in COVID-19 patients.Annals of medicine · 2025Article
- TGF-β inhibitor SB431542 suppresses SARS-CoV-2 replication through multistep inhibition.Journal of virology · 2025Article
- SARS-CoV-2 N protein induces hypokalemia in acute kidney injury mice via ENaC-dependent mechanism.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Insulin like growth factor binding protein 7 activate JNK/ERK signaling to aggravate uranium-induced renal cell cytotoxicity.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Targeting USP22 to promote K63-linked ubiquitination and degradation of SARS-CoV-2 nucleocapsid protein.Journal of virology · 2025Article
- SARS-CoV-2 nucleocapsid protein induces a Mincle-dependent macrophage inflammatory response in acute kidney injury.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Enzyme-Responsive Nanoparachute for Targeted miRNA Delivery: A Protective Strategy Against Acute Liver and Kidney Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- SARS-CoV-2 specific adaptations in N protein inhibit NF-κB activation and alter pathogenesis.The Journal of cell biology · 2025Article
- Coronavirus nucleocapsid proteins: a multifaceted modulator in the innate immune evasion.Frontiers in microbiology · 2025Review
- Smad3 Mediates Renal Fibrosis via GPX4-Dependent Ferroptosis.International journal of biological sciences · 2025Article
- A genome-wide association study identifies new loci associated with response to SARS-CoV-2 mRNA-1273 vaccine in a cohort of healthy healthcare workers.Frontiers in immunology · 2025Article
- Pathological Sequelae of SARS-CoV-2: A Review for Clinicians.The Yale journal of biology and medicine · 2024Review
- Article
- TGF‑β/Smad signaling in chronic kidney disease: Exploring post‑translational regulatory perspectives (Review).Molecular medicine reports · 2024Review
- Article
- P53-Independent G1-Cell Cycle Arrest Increases SARS-CoV-2 RNA Replication.Microorganisms · 2024Article
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
COVID-19 is infected by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and can cause severe multiple organ injury and death. Kidney is one of major target organs of COVID-19 and acute kidney injury (AKI) is common in critically ill COVID-19 patients. However, mechanisms through which COVID-19 causes AKI remain largely unknown and treatment remains unspecific and ineffective. Here, the authors report that normal kidney-specifically overexpressing SARS-CoV-2 N develops AKI, which worsens in mice under ischemic condition. Mechanistically, it is uncovered that SARS-CoV-2 N-induced AKI is Smad3-dependent as SARS-CoV-2 N protein can interact with Smad3 and enhance TGF-β/Smad3 signaling to cause tubular epithelial cell death and AKI via the G1 cell cycle arrest mechanism. This is further confirmed in Smad3 knockout mice and cells in which deletion of Smad3 protects against SARS-CoV-2 N protein-induced cell death and AKI in vivo and in vitro. Most significantly, it is also found that targeting Smad3 with a Smad3 pharmacological inhibitor is able to inhibit SARS-CoV-2 N-induced AKI. In conclusion, the authors identify that SARS-CoV-2 N protein is a key mediator for AKI and induces AKI via the Smad3-dependent G1 cell cycle arrest mechanism. Targeting Smad3 may represent as a novel therapy for COVID-19-asscoaited AKI.
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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 Socratic graph.