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• W4311448216 abstract "<b><i>Background:</i></b> C-reactive protein (CRP) is an acute-phase protein and has been found to be a risk factor for acute kidney injury (AKI) and chronic kidney diseases (CKD). However, the role and mechanisms of CRP in AKI and CKD remain largely unclear. <b><i>Summary:</i></b> Clinically, elevated serum CRP is a risk factor or biomarker for patients with AKI and CKD. Interestingly, in critically ill COVID-19 patients, increased serum CRP is also associated with the development of AKI. Functionally, studies using human CRP transgenic mouse models find that CRP is pathogenic and can function as a mediator for AKI and CKD as mice overexpressing human CRP promote AKI and CKD. Mechanistically, CRP can promote AKI and CKD via NF-κB and Smad3-dependent mechanisms. We found that CRP can activate Smad3 signaling directly and cause AKI via the Smad3-p27-dependent G1 cell cycle arrest mechanism. Thus, targeting CRP-Smad3 signaling with a neutralizing antibody or Smad3 inhibitor can inhibit AKI. <b><i>Key Messages:</i></b> CRP acts not only as a biomarker but also as a mediator for AKI and CKD. CRP can activate Smad3 to induce cell death and cause progressive renal fibrosis. Thus, targeting CRP-Smad3 signaling may represent a promising therapy for AKI and CKD." @default.
• W4311448216 created "2022-12-26" @default.
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• W4311448216 date "2022-12-14" @default.
• W4311448216 modified "2023-10-18" @default.
• W4311448216 title "Role of C-Reactive Protein in Kidney Diseases" @default.
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• W4311448216 doi "https://doi.org/10.1159/000528693" @default.
• W4311448216 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/37065607" @default.
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