Monomeric C-reactive Protein as a Mediator of Chronic Inflammation in Obesity

Obesity is associated with persistent low-grade inflammation. This inflammation results from interactions between adipose tissue, immune cells, and metabolic pathways. High-sensitivity C-reactive protein (CRP) serves as a marker for systemic inflammation but does not evaluate local inflammatory processes. Recent findings indicate that the monomeric variant of CRP is biologically active and may contribute to inflammation in multiple tissues, including adipose tissue. This review examines the role of monomeric CRP (mCRP) as a mediator of ongoing inflammation in obesity and discusses the mechanisms through which it contributes to endothelial dysfunction, immune activation, and metabolic changes. We created a narrative review utilizing the PubMed electronic database. Relevant research on CRP isoforms, mCRP development, cellular targets, and their involvement in obesity-related inflammation was included and examined. mCRP forms locally under conditions such as oxidative stress, membrane injury, and cellular activation and may trigger proinflammatory effects in the endothelium, macrophages, platelets, and adipose tissue. mCRP may stimulate the endothelium, leading to heightened expression of adhesion molecules. This aids in leukocyte recruitment and reduces nitric oxide availability. mCRP may encourage macrophage polarization toward a proinflammatory type and enhance the formation of neutrophil extracellular structures. At the level of platelets, it has been shown to increase platelet aggregation and may aid in thrombus stabilization. Moreover, mCRP has been associated with increased reactive oxygen species production in experimental settings, creating a loop of inflammatory amplification. mCRP could disrupt leptin signaling and may contribute to leptin resistance. The conclusions of this review suggest that mCRP acts as an active mediator of chronic inflammation associated with obesity. It is more than a passive biomarker, as localized production may amplify tissue-level inflammatory effects. This may explain the disparity between systemic inflammatory indicators and ongoing vascular and metabolic inflammation. Additional studies are needed to standardize detection techniques and to define their clinical significance in risk assessment and treatment strategies.