2020
DOI: 10.1007/s10753-020-01368-w
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Mono-macrophage-Derived MANF Protects Against Lipopolysaccharide-Induced Acute Kidney Injury via Inhibiting Inflammation and Renal M1 Macrophages

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Cited by 24 publications
(20 citation statements)
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“…MANF also promotes immune cell phenotype switch from proinflammatory macrophages to pro-repair anti-inflammatory macrophages [ 49 ]. MANF is therefore considered as a negative regulator of inflammation [ 52 ]. Further, restoring MANF levels can extend fly lifespan, reverse liver damage and inflammation in old mice by regulating metabolic and immune homeostasis in ageing [ 49 , 53 ].…”
Section: Discussionmentioning
confidence: 99%
“…MANF also promotes immune cell phenotype switch from proinflammatory macrophages to pro-repair anti-inflammatory macrophages [ 49 ]. MANF is therefore considered as a negative regulator of inflammation [ 52 ]. Further, restoring MANF levels can extend fly lifespan, reverse liver damage and inflammation in old mice by regulating metabolic and immune homeostasis in ageing [ 49 , 53 ].…”
Section: Discussionmentioning
confidence: 99%
“…Specifically, in response to retinal damage signals, the expression of MANF is transiently induced in innate immune cells and immune cell-derived MANF promotes a phenotype switch of macrophages from proinflammatory to anti-inflammatory in an autocrine manner [47] (Figure 2). Moreover, studies also showed that MANF knockout in mouse monomacrophages increased splenic [48], renal [49], and myocardial [50] M1-macrophages, whereas another study found that MANF transiently increased the number of phagocytic innate immune cells to promote functional recovery in post-stroke rats but did not recruit alternatively activated macrophages [51].…”
Section: Open Accessmentioning
confidence: 99%
“…All the above can be regarded as characteristics of M1 macrophages. Meanwhile, M1 macrophages showed stronger phagocytosis and antigen-presenting ability, which could eliminate the necrotic cells ( Hou et al, 2020 ). However, excessive secretion of pro-inflammatory cytokines, reactive oxygen species (ROS), and reactive nitrogen species (RNS) after M1 cell polarization can impair neurons and glia and even cause more serious neuron apoptosis ( Block et al, 2007 ).…”
Section: Hematogenous Macrophages Participate In Spinal Cord Injury Pathologymentioning
confidence: 99%