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C-reactive protein and ageing
Ying Tang1, Erik Fung2, Anping Xu1
1Department of Nephrology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, China.
Insights
C-reactive protein (CRP) is an inflammatory biomarker and risk factor in aging-related diseases. It drives inflammation, fibrosis, and impairs cell regeneration, contributing to aging and disease progression.
Area of Science:
- Biochemistry
- Immunology
- Gerontology
Background:
- C-reactive protein (CRP) is increasingly recognized beyond its role as an inflammatory biomarker.
- Emerging evidence links CRP to various age-related diseases, including cardiovascular, hypertensive, diabetic, and kidney conditions.
- CRP's pathogenic roles in diseases like hypertensive complications and diabetic nephropathy are being elucidated.
Purpose of the Study:
- To review the multifaceted roles of C-reactive protein (CRP) in the aging process.
- To explore CRP's mechanisms in physiological aging and age-related diseases.
- To detail CRP's impact on cellular signaling pathways relevant to aging.
Main Methods:
- Literature review of recent studies on CRP's function and mechanisms.
- Analysis of CRP's involvement in inflammatory and fibrotic pathways.
- Examination of CRP's effects on cell cycle regulation and aging.
Main Results:
- CRP acts as a pathogenic factor in cardiovascular and kidney diseases.
- CRP activates key signaling pathways including NF-κB, TGF-β/Smad, and mTOR.
- CRP impairs cell regeneration by inducing cell cycle arrest and promotes aging via Smad3-dependent mechanisms.
Conclusions:
- CRP is a significant contributor to aging and age-related pathologies.
- Understanding CRP's signaling mechanisms offers therapeutic targets for aging and related diseases.
- CRP's role extends to cellular processes, impacting regeneration and senescence.
Abstract:
Increasing evidence shows that C-reactive protein (CRP) is not only an inflammatory biomarker but also an important risk factor associated with ageing-related diseases including cardiovascular disease, hypertension, diabetes mellitus, and kidney disease. Recent studies have demonstrated that CRP is pathogenic in a number of diseases including hypertensive cardiovascular and kidney complications, diabetic nephropathy, and acute and chronic kidney diseases. It is well known that CRP binds its receptor, CD32/CD64, to induce the process of inflammation by activating the NF-κB signalling pathway. In addition, CRP mediates tissue fibrosis in a number of cardiovascular and kidney diseases by activating TGF-β/Smad signalling via TGF-β1-dependent and independent mechanisms. Furthermore, CRP is able to activate mTOR signalling in the diabetic conditions. Our recent studies also revealed that CRP impairs cell regeneration by causing the G1 cell cycle arrest and promotes ageing via a Smad3-dependent p21/p27 mechanism. In this review, we discuss the roles of CRP in ageing, with a focus on its function and mechanisms in physiological or "healthy" ageing, in ageing-related diseases, and in cell signalling.