Fgr, a member of the Src family of tyrosine kinases, is involved in the innate immune response, hematologic cancer, diet-induced obesity, and hemorrhage-induced thalamic pain. It is expressed in cells like peripheral-blood granulocytes, monocytes, tissue macrophages, and its expression is activated in Epstein-Barr-virus-infected B lymphocytes [2].

In a cecal ligation and puncture (CLP)-induced mouse sepsis model, CLP-induced sepsis increased the expression of Fgr in hippocampal neurons. Pharmacological inhibition of Fgr attenuated CLP-induced neuroinflammation, improved the survival rate, and alleviated cognitive and emotional dysfunction, oxidative stress, and mitochondrial dysfunction. Fgr interacted with SIRT1 and reduced its activity and expression, and activation of SIRT1/PGC-1α promoted the protective effects of the Fgr inhibitor on CLP-induced brain dysfunction [1]. In radiation-induced pulmonary fibrosis (RIPF) mouse models, inhibition of Fgr by TL02-59 reduced the release of profibrotic chemokines from the lungs of RIPF mice, prevented RIPF, significantly reduced levels of expression of fibrotic gene products, and the recruitment of CD11b+ macrophages to the lungs [3].

In conclusion, Fgr plays significant roles in processes related to sepsis-associated encephalopathy and radiation-induced pulmonary fibrosis. Studies using mouse models, such as the CLP-induced sepsis model and RIPF mouse models, have revealed its involvement in neuroinflammation, oxidative stress, mitochondrial function, and pulmonary fibrosis-related pathways. Understanding Fgr's functions can potentially lead to new therapeutic strategies for these disease conditions.