C3, also known as Complement 3, is the central effector molecule of the complement system [1]. It is crucial for the innate immune system, playing a key role in the detection and clearance of potential pathogens by interacting with other complement proteins [6]. C3 is at the nexus of all complement activation pathways, and its activation fragments and receptors trigger a complex network of downstream effects [4].

In C3 glomerulopathy (C3G), an uncontrolled overactivation of the alternative complement pathway occurs, leading to abnormal C3 deposition in the glomeruli and progression of renal damage [2,3,5]. In C3 glomerulonephritis (C3 GN), a subtype of C3G, abnormal activation of the alternative pathway of the complement system results in predominant C3 deposition in glomeruli [8]. Additionally, in gastric cancer, C3+ cancer-associated fibroblasts promote tumor growth, therapeutic resistance, epithelial-mesenchymal transition, and immunosuppressive effects via activation of the NF-κB signaling pathway [7].

In conclusion, C3 is essential for the normal function of the complement system in the innate immune response. Studies on diseases like C3G, C3 GN, and gastric cancer have highlighted the significance of C3 in disease pathogenesis. Understanding C3's role through these disease models provides insights into potential therapeutic strategies for complement-mediated diseases.