Organ transplantation is the optimal treatment for end-stage organ failure. Nevertheless, rejection remains an important factor affecting the allograft survival. At present, acute rejection may be effectively treated, whereas no effective interventions are available for post-transplantation chronic rejection. Long-term chronic rejection may lead to graft failure and severely affect long-term survival rate of allografts. In recent years, the role of macrophages in post-transplantation chronic rejection has gradually captivated increasing attention. In this article, main pathological changes of chronic rejection, the diversity and functional differences of macrophages involved in chronic rejection, and the role and mechanism of macrophages in chronic rejection were reviewed, and research progresses on macrophage-related treatment for chronic rejection were summarized, aiming to provide reference for the study of macrophages in post-transplantation chronic rejection.

Ischemia-reperfusion injury, rejection, nephrotoxicity caused by calcineurin inhibitors and other factors cause excessive accumulation of renal extracellular matrix after kidney transplantation, which gradually induce renal fibrosis and eventually lead to renal failure. In recent years, the mechanism of macrophages in renal allograft fibrosis has gradually captivated widespread attention. Studies have shown that some drugs like mammalian target of rapamycin inhibitors may mitigate renal allograft fibrosis through the macrophage. In this article, the main pathogenesis and pathophysiological mechanism of renal allograft fibrosis, the role of different macrophages in the progression of renal allograft fibrosis, the infiltration of peripherally-recruited macrophages and renal resident macrophages into renal injury areas, the induction of myofibroblasts by macrophages and potential treatment regimens of macrophage-associated renal allograft fibrosis were reviewed, aiming to provide reference for investigating the role of macrophages in renal allograft fibrosis.

Objective : To investigate the effects of melatonin ( MEL) on the proliferation of hepatic stellate cells (HSCs) induced by platelet - derived growth factor (PDGF⁃BB) and explore its correlation with the regulation of autophagy levels . Methods : The HSC⁃T6 cells were divided into the following groups : control group , model group and MEL (low , medium and high) treatment groups . After 24 hours culture , the cells adhered to the wall and were changed into serum⁃free DMEM medium to synchronize the cells to the G0 stage . After 24 hours culture , all groups were given with PDGF ⁃ BB ( 10 ng/ml) excepted the control group . Besides , melatonin of different concentrations ( 1 nmol/L , 1 μmol/L and 0. 1 mmol/L) were added immediately in three treated groups . After incubated for 48 hours , the effect of MEL on the proliferation of hepatic stellate cells activated by PDGF⁃BB was detected by CCK8 method . The protein expression levels of LC3b and α ⁃SMA in hepatic stellate cells were determined by Western blot . The expression levels of LC3b mRNA and α ⁃SMA mRNA in hepatic stellate cells were determined by qRT⁃PCR . The ultrastructure of HSCs was observed by transmission electron microscopy to understand the autophagy level. Results : Compared with control group , PDGF⁃BB could induce the proliferation of HSCs ( P < 0. 01) . Compared with model group , MEL inhibited the proliferation of HSCs activated by PDGF⁃BB ( P < 0. 01) . Compared with the control group , LC3b and α ⁃SMA protein expressions significantly increased in the model group ( all P < 0. 05) , and LC3b mRNA and α ⁃SMA mRNA expressions significantly increased in the model group (P < 0. 05 , P < 0. 01) . Compared with the model group , MEL could inhibit such effects (LC3b : P < 0. 05 , P < 0. 01 ; α ⁃SMA : P < 0. 01) . Transmission electron microscopy ( TEM) showed that compared with the control group , autopolysosome significantly increased in the model group (P < 0. 05) . Compared with model group , autopolysosome significantly decreased in MEL treatment group (P < 0. 01) . Conclusion The up⁃regulation of autophagy level can promote the proliferation of hepatic stellate cells and the inhibition of hepatic stellate cell proliferation by MEL may be related to the down⁃regulation of autophagy level .