Clec7a, also known as Dectin-1, is a pattern recognition receptor involved in various biological processes. It is associated with the recognition of fungi and plays a role in innate immune responses, especially in processes related to phagocytosis and inflammation [3,7]. Clec7a can directly activate SYK, which is involved in intracellular signaling pathways [4].

In disease models, Clec7a has shown significant impacts. In an ischemic stroke mouse model, manipulating microglial Clec7a expression regulated microglial phagocytosis of synapses, with Clec7a knockdown alleviating injury by inhibiting pyroptosis and microglial activation, suggesting it may be a therapeutic target for stroke [1,5]. In a Parkinson's disease model, AAV-mediated specific knockdown of Clec7a in microglial alleviated motor deficits and dopaminergic neuron damage, restraining neuroinflammation [6]. In an acute kidney injury model, combined expression of Clec7a in M1 macrophages and depletion in M2 macrophages improved renal function, indicating its role in macrophage phenotype regulation during AKI [2].

In conclusion, Clec7a is crucial in processes like phagocytosis and inflammation. Gene knockout or knockdown studies in mouse models for diseases such as ischemic stroke, Parkinson's disease, and acute kidney injury have revealed its potential as a therapeutic target. These models help us understand how Clec7a contributes to disease pathogenesis, providing insights for developing new treatment strategies.