Table 2.

Selected mechanisms of interactions between GLP-1R agonists, inflammation and oxidative stress.

	Inflammation	Oxidative Stress
	Kidney
GLP-1R agonists	-Suppress NF-κB [89] -Normalize expression of TNFα, IL-1β, TGFβ, fibronectin, inhibit chemokines attracting macrophages to the site of injury and promoting their infiltration (MCP-1, ICAM-1) [88,89,91,92,93,96,102,104] -Inhibit transition of cultured mesangial cells into fibroblast-like phenotype (with concomitant inhibition of TGFβ1-signaling) [92] -Downregulate RAGE expression on mesangial cells [96] -Increase the Wnt/β-catenin signaling resulting in reduction of ECM protein synthesis [98] -Reverse downregulation of SIRT-1 [99] -Decrease the mRNA expression of collagen type I alpha 1 chain (the marker of fibrosis), reduce the renal infiltrates with PMN, macrophages, T-helper cells and cytotoxic T lymphocytes; reduce gene expression of IFγ, TNFα and T-bet [104,105]	-Decrease 8-hydroxydeoxyguanosine content, mRNA of NADPH 4 oxidase (NOX4) and NOX4 protein expression [88,89,93,100] -Inhibit NADPH oxidase activity [93] -Decrease reactive oxygen species generation and MDA production [89,91,93] -Restore content of catalase and glutathione peroxidase-3 [90] -Decrease expression of renal iNOS and COX-2 [91]
	Other organs/tissues/cells
GLP-1R agonists	-Adipocytes: decrease levels of IL-6 and MCP1 mRNA [108] -Adipocytes: increase translocation of the transcription factor Forkhead Box O1 (Foxo1) from cytoplasm to the nucleus [109] -PBMC: suppress secretion of chemokines CCL5 and CXCL10 [110] -PBMC: decrease levels of phosphorylated kinases: phos-ERK and phos-p38 MAPK [110] -PBMC: suppress NFκB, reduce mRNA of TNFα and IL-1β [111,112,116] -PBMC: suppress mRNA of c-JUN N- terminal kinase (JNK1), toll-like receptors (TLR) 2 and 4 [111] -Monocytes: reduce expression of mRNA for ICAM1, VCAM1, TNFα and MCP1 in these cells [112] -Macrophages: promoted an activation of signal transducer and activator of transcription 3 (STAT3), followed by increased expression of IL-10 [114,116] -Macrophages: reverse macrophage shift from M1 towards M2 [116] -Decrease number of peripheral regulatory T cells (Treg) [115] -Cardiomyocytes/liver: promote autophagy—activation (phosphorylation) of AMPK and inactivation of mTOR [117,118] -Cardiomyoblasts: increase cAMP content in the cells [119]	-PBMC: decrease ROS generation [111] -Cardiomyoblasts: decrease mitochondrial ROS generation and stabilizes mitochondrial membrane potential [119] -Cardiomyoblasts: decrease reactive oxygen species production [123] -Cardiomyocytes: increase expression of MnSOD and catalase [123]