2 results match your criteria: "Third Affifiliated Hospital of Sun Yat-sen University[Affiliation]"
CX3CR1 deficiency promotes resolution of hepatic ischemia-reperfusion injury by regulating homeostatic function of liver infiltrating macrophages.
Biochim Biophys Acta Mol Basis Dis
June 2024
Department of Hepatic Surgery and Liver Transplantation Center, the Third Affiliated Hospital of Sun Yat-sen University, Organ Transplantation Institute, Sun Yat-sen University, Organ Transplantation Research Center of Guangdong Province, Guangdong Province Engineering Laboratory for Transplantation Medicine, Guangzhou, China; Guangdong Key Laboratory of Liver Disease Research, the Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China; Key Laboratory of Liver Disease Biotherapy and Translational Medicine of Guangdong Higher Education Institutes, the Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, China. Electronic address:
Article Synopsis
- Hepatic ischemia-reperfusion injury (HIRI) is a problem that can lead to organ failure after liver surgery, and the study looks at how certain proteins affect this issue.
- The researchers found that lower levels of a protein called CX3CR1 are linked to better recovery of damaged liver tissue during transplants.
- By studying mice and using different tests, they discovered that blocking CX3CR1 can help improve the healing process after liver injury by allowing more immune cells to move to the damaged area.
Pathogenesis and treatment of neuropsychiatric systemic lupus erythematosus: A review.
Front Cell Dev Biol
September 2022
Department of Rheumatology, Third Affifiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Systemic lupus erythematosus (SLE) is an autoimmune inflammatory disease with a complex pathogenesis. Neuropsychiatric systemic lupus erythematosus (NPSLE) is a serious complication of SLE that involves the nervous system and produces neurological or psychiatric symptoms. After decades of research, it is now believed that the diverse clinical manifestations of NPSLE are associated with intricate mechanisms, and that genetic factors, blood-brain barrier dysfunction, vascular lesions, multiple autoimmune antibodies, cytokines, and neuronal cell death may all contribute to the development of NPSLE.
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