ArticleJournal of molecular cell biology2021
Kidney injury molecule-1 is a potential receptor for SARS-CoV-2.
Article in Journal of molecular cell biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 67 citations in OpenAlex.
- Bridging structure and function: artificial intelligence-based modelling of kidney proteins.Nature reviews. Nephrology · 2026Review
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- Exploration of immune phenotypes in self-sampling citizens.iScience · 2026Article
- Tumor Targeting with Peptide-Drug Conjugates: Showcasing Key Progress and Hurdles.Drug design, development and therapy · 2026Review
- Chemically Synthesized LRAD3-D1 Interacts with N-Terminal Domain of SARS-CoV-2 Spike Protein.Chembiochem : a European journal of chemical biology · 2025Article
- Molecular mechanisms of SARS-CoV-2 entry: implications for biomedical strategies.Microbiology and molecular biology reviews : MMBR · 2025Review
- A rationally designed injury kidney targeting peptide library and its application in rescuing acute kidney injury.Science advances · 2025Article
- Trends in the research and development of peptide drug conjugates: artificial intelligence aided design.Frontiers in pharmacology · 2025Review
- β-synuclein regulates the phase transitions and amyloid conversion of α-synuclein.Nature communications · 2024Article
- Article
- Aprotinin (I): Understanding the Role of Host Proteases in COVID-19 and the Importance of Pharmacologically Regulating Their Function.International journal of molecular sciences · 2024Review
- Kidney organoids reveal redundancy in viral entry pathways during ACE2-dependent SARS-CoV-2 infection.Journal of virology · 2024Article
- The Role of Extracellular Vesicles in SARS-CoV-2-Induced Acute Kidney Injury: An Overview.Life (Basel, Switzerland) · 2024Review
- ANGPTL3 negatively regulates IL-1β-induced NF-κB activation by inhibiting the IL1R1-associated signaling complex assembly.Journal of molecular cell biology · 2024Article
- Potential Alternative Receptors for SARS-CoV-2-Induced Kidney Damage: TLR-4, KIM-1/TIM-1, and CD147.Frontiers in bioscience (Landmark edition) · 2024Review
- ISG15 accelerates acute kidney injury and the subsequent AKI-to-CKD transition by promoting TGFβR1 ISGylation.Theranostics · 2024Article
- COVID-19 and Kidney: The Importance of Follow-Up and Long-Term Screening.Life (Basel, Switzerland) · 2023Review
- A disintegrin and metalloproteinase domain 9 facilitates SARS-CoV-2 entry into cells with low ACE2 expression.Microbiology spectrum · 2023Article
- A renal YY1-KIM1-DR5 axis regulates the progression of acute kidney injury.Nature communications · 2023Article
- Loss of renal tubular G9a benefits acute kidney injury by lowering focal lipid accumulation via CES1.EMBO reports · 2023Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
COVID-19 patients present high incidence of kidney abnormalities, which are associated with poor prognosis and mortality. The identification of SARS-CoV-2 in the kidney of COVID-19 patients suggests renal tropism of SARS-CoV-2. However, whether there is a specific target of SARS-CoV-2 in the kidney remains unclear. Herein, by using in silico simulation, coimmunoprecipitation, fluorescence resonance energy transfer, fluorescein isothiocyanate labeling, and rational design of antagonist peptides, we demonstrate that kidney injury molecule-1 (KIM1), a molecule dramatically upregulated upon kidney injury, binds with the receptor-binding domain (RBD) of SARS-CoV-2 and facilitates its attachment to cell membrane, with the immunoglobulin variable Ig-like (Ig V) domain of KIM1 playing a key role in this recognition. The interaction between SARS-CoV-2 RBD and KIM1 is potently blockaded by a rationally designed KIM1-derived polypeptide AP2. In addition, our results also suggest interactions between KIM1 Ig V domain and the RBDs of SARS-CoV and MERS-CoV, pathogens of two severe infectious respiratory diseases. Together, these findings suggest KIM1 as a novel receptor for SARS-CoV-2 and other coronaviruses. We propose that KIM1 may thus mediate and exacerbate the renal infection of SARS-CoV-2 in a 'vicious cycle', and KIM1 could be further explored as a therapeutic target.
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