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<p>An important part of the pathophysiology of atherosclerosis is the involvement of inflammatory processes, which mediate various stages of the formation of atheroma, from the first leukocyte recruitment to the final rupture of the unstable atherosclerotic plaque. Acute phase reactant C-reactive protein (CRP), which represents varying degrees of inflammation, has been identified as a separate risk factor for several cardiovascular diseases (CVD), particularly unstable coronary syndrome. We hypothesize that CRP is a direct cause of CVD in addition to being an inflammatory marker. Therefore, therapies aimed at lowering CRP should be beneficial for both primary and secondary CVD prevention. It has been demonstrated that the use of many drugs, particularly statins, alters CRP levels while also lowering cardiovascular events. The use of inflammatory biomarkers aids in the discovery of CVDs and tracks the assessment, prognosis, and administration of treatment. An acute-phase protein called C-reactive protein (CRP) is created in response to pro-inflammatory cytokines. CRP is a key modulator of atherosclerosis and a biomarker of the inflammatory response. It is also regarded as a CVD risk factor since it actively promotes the growth of atherosclerotic plaque, instability, and consequent clot. Patients with intermediate risk for cardiovascular diseases have been using the plasma concentration of hsCRP (high sensitivity CRP) as a biomarker for disease prognosis since 2010.</p>

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Impact of NSAIDs corticosteroids DMARDs biologics and their comparisons with natural products in C-reactive proteins (CRP) linked cardiovascular disorders

  • 期刊论文

  • 发表日期：

    2025年5月4日

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  • Trilochan Satapathy,
  • Anjali Minj,
  • Mansi Verma

摘要

An important part of the pathophysiology of atherosclerosis is the involvement of inflammatory processes, which mediate various stages of the formation of atheroma, from the first leukocyte recruitment to the final rupture of the unstable atherosclerotic plaque. Acute phase reactant C-reactive protein (CRP), which represents varying degrees of inflammation, has been identified as a separate risk factor for several cardiovascular diseases (CVD), particularly unstable coronary syndrome. We hypothesize that CRP is a direct cause of CVD in addition to being an inflammatory marker. Therefore, therapies aimed at lowering CRP should be beneficial for both primary and secondary CVD prevention. It has been demonstrated that the use of many drugs, particularly statins, alters CRP levels while also lowering cardiovascular events. The use of inflammatory biomarkers aids in the discovery of CVDs and tracks the assessment, prognosis, and administration of treatment. An acute-phase protein called C-reactive protein (CRP) is created in response to pro-inflammatory cytokines. CRP is a key modulator of atherosclerosis and a biomarker of the inflammatory response. It is also regarded as a CVD risk factor since it actively promotes the growth of atherosclerotic plaque, instability, and consequent clot. Patients with intermediate risk for cardiovascular diseases have been using the plasma concentration of hsCRP (high sensitivity CRP) as a biomarker for disease prognosis since 2010.