Macrophages in Renal Fibrosis

Meng, Xiao‐Ming; Mak, Tony; Lan, Hui‐Yao

doi:10.1007/978-981-13-8871-2_13

Cited by 47 publications

(60 citation statements)

References 142 publications

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“…AKI is associated with intra-renal and systemic inflammation. Thus, improved understanding of the cellular mechanisms underlying the inflammatory response has the potential to identify effective therapies to ameliorate AKI (6,24,25). It was demonstrated that macrophages are a major contributor to the inflammatory response in the AKI animal model.…”

Section: Discussionmentioning

confidence: 99%

“…However, its clinical application is limited by time-and dose-dependent nephrotoxicity, which is associated with high morbidity and mortality (3,4). Inflammation is reported to be involved in the development and amplification of kidney injury (5,6). Recent studies revealed that activation of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) plays a decisive role in nephrotoxicity by inducing a variety of signaling pathways.…”

Section: Introductionmentioning

confidence: 99%

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Inhibition of Histone H3K27 Acetylation Orchestrates Interleukin-9-Mediated and Plays an Anti-Inflammatory Role in Cisplatin-Induced Acute Kidney Injury

et al. 2020

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Nephrotoxicity is a major side effect of cisplatin (CP)-and platinum-related chemotherapy, and inflammation contributes to disease pathogenesis. Interleukin-9 (IL-9) is a pleiotropic cytokine associated with inflammation. Here, we investigated the key role of IL-9 as a regulator of protective mechanisms in CP-induced acute kidney injury (AKI). We observed that IL-9 was decreased not only in a CP-induced AKI mouse model but also in THP-1 and RAW264.7 cell lines. Seventy-two hours post-CP injection, renal dysfunction and tubule injury were significantly attenuated in IL-9 overexpression adeno-associated virus 9 (AAV9)-treated mice. The levels of serum urea, serum creatinine, kidney injury molecule-1 (KIM-1), and histological damage were partially diminished following treatment with IL-9. The renoprotective effects of IL-9 may be attributed to the regulation of cytokines, and we found that IL-9 acted on macrophages in a regulatory manner, promoting an anti-inflammatory phenotype. Furthermore, IL-9 enhanced the suppression of macrophage-driven renal inflammation. Inhibition of H3K27 acetylation orchestrated IL-9-mediated renoprotection in CP-induced AKI. Thus, our findings indicate novel and potent anti-inflammatory properties of IL-9 that confer preservation of kidney function and structure in CP-induced AKI, which may counteract kidney disease procession.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Inhibition of Histone H3K27 Acetylation Orchestrates Interleukin-9-Mediated and Plays an Anti-Inflammatory Role in Cisplatin-Induced Acute Kidney Injury

et al. 2020

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“…Inflammatory renal damages and fibrosis are closely related to macrophage polarization in the kidney (Meng et al, 2019).…”

Section: Tfa and Feb Modulate Macrophage Polarization In Vivo And In mentioning

confidence: 99%

Total Flavones of Abelmoschus manihot Remodels Gut Microbiota and Inhibits Microinflammation in Chronic Renal Failure Progression by Targeting Autophagy-Mediated Macrophage Polarization

Fang

Sun

et al. 2020

Front. Pharmacol.

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oxidase, serine racemase, D-serine, and L-serine; inhibited microinflammation, including interleukin 1b (IL1b), tumor necrosis factor-a, and nuclear factor-kB; and modulated macrophage polarization, including markers of M1/M2 macrophages. More importantly, TFA and FEB reversed the expression of beclin1 (BECN1) and phosphorylation of p62 protein and light chain 3 (LC3) conversion in the kidneys by activating the adenosine monophosphate-activated protein kinase-sirtuin 1 (AMPK-SIRT1) signaling. Further, TFA and FEB have similar effects on macrophage polarization and autophagy and its related signaling in vitro. Conclusion: In this study, we demonstrated that TFA, similar to FEB, exerts its renoprotective effects partially by therapeutically remodeling gut microbiota dysbiosis and inhibiting intestinal metabolite-derived microinflammation. This is achieved by adjusting autophagy-mediated macrophage polarization through AMPK-SIRT1 signaling. These findings provide more accurate information on the role of TFA in delaying CRF progression.

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“…In recent years the role of immune cells in the renal fibrosis process has become very relevant, especially monocyte/macrophage function [65][66][67]. Initially during renal damage, macrophages can acquire a phenotype known as M1 (iNOS+/CD80+/CCR7+) which favors a pro-inflammatory microenvironment [66].…”

Section: Discussionmentioning

confidence: 99%

Intraglomerular Monocyte/Macrophage Infiltration and Macrophage–Myofibroblast Transition during Diabetic Nephropathy Is Regulated by the A2B Adenosine Receptor

Torres

Muñoz

Nahuelpán

et al. 2020

Cells

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Diabetic nephropathy (DN) is considered the main cause of kidney disease in which myofibroblasts lead to renal fibrosis. Macrophages were recently identified as the major source of myofibroblasts in a process known as macrophage-myofibroblast transition (MMT). Adenosine levels increase during DN and in vivo administration of MRS1754, an antagonist of the A 2B adenosine receptor (A 2B AR), attenuated glomerular fibrosis (glomerulosclerosis). We aimed to investigate the association between A 2B AR and MMT in glomerulosclerosis during DN. Kidneys/glomeruli of non-diabetic, diabetic, and MRS1754-treated diabetic (DM+MRS1754) rats were processed for histopathologic, transcriptomic, flow cytometry, and cellular in vitro analyses. Macrophages were used for in vitro cell migration/transmigration assays and MMT studies. In vivo MRS1754 treatment attenuated the clinical and histopathological signs of glomerulosclerosis in DN rats. Transcriptomic analysis demonstrated a decrease in chemokine-chemoattractants/cell-adhesion genes of monocytes/macrophages in DM+MRS1754 glomeruli. The number of intraglomerular infiltrated macrophages and MMT cells increased in diabetic rats. This was reverted by MRS1754 treatment. In vitro cell migration/transmigration decreased in macrophages treated with MRS1754. Human macrophages cultured with adenosine and/or TGF-β induced MMT, a process which was reduced by MRS1754. We concluded that pharmacologic blockade of A 2B AR attenuated some clinical signs of renal dysfunction and glomerulosclerosis, and decreased intraglomerular macrophage infiltration and MMT in DN rats.Cells 2020, 9, 1051 2 of 21 that affects close to 50% of patients with chronic kidney disease (CKD) and end-stage renal disease (ESRD) [3,7]. During DN, patients lose glomerular function. This is clinically manifested by the appearance of proteins in the urine (proteinuria; an albumin excretion rate ≥300 mg/24 h per gram of creatinine) and/or a reduced glomerular filtration rate (GFR; below 60 mL/min/1.73 m 2 ) [2]. In addition, people with DN who reach the stage of CKD [8] show an increase in the production of urine (polyuria), the appearance of glucose in the urine (glycosuria), and an increase in blood urea nitrogen (BUN) and serum creatinine [9]. Currently, management of DN patients involves the use of antihypertensive, antidyslipidemic, and antidiabetic agents, however these drugs have only shown a modest efficacy in slowing the evolution of the disease [10]. Regardless of the treatment used, the progression of DN leads to renal fibrosis [11], which irreversibly remodels the parenchyma tissue replacing it with extracellular matrix (ECM), thereby losing functionality [12]. Renal fibrosis predisposes patients to organ replacement therapies, such as hemodialysis and kidney transplantation, which means serious economic and societal costs for health systems [1,2,[13][14][15]. The pathophysiological events that trigger renal fibrosis are still unknown, however, this process is orchestrated by myofibroblasts, cells which have the ca...

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Macrophages in Renal Fibrosis

Cited by 47 publications

References 142 publications

Inhibition of Histone H3K27 Acetylation Orchestrates Interleukin-9-Mediated and Plays an Anti-Inflammatory Role in Cisplatin-Induced Acute Kidney Injury

Inhibition of Histone H3K27 Acetylation Orchestrates Interleukin-9-Mediated and Plays an Anti-Inflammatory Role in Cisplatin-Induced Acute Kidney Injury

Total Flavones of Abelmoschus manihot Remodels Gut Microbiota and Inhibits Microinflammation in Chronic Renal Failure Progression by Targeting Autophagy-Mediated Macrophage Polarization

Intraglomerular Monocyte/Macrophage Infiltration and Macrophage–Myofibroblast Transition during Diabetic Nephropathy Is Regulated by the A2B Adenosine Receptor

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