nach oben

Inflammation Research

Erschienen in:

24.05.2020 | Review

Inflammasome activation in podocytes: a new mechanism of glomerular diseases

verfasst von: Wei Xiong, Xian-Fang Meng, Chun Zhang

Erschienen in: Inflammation Research | Ausgabe 8/2020

Einloggen, um Zugang zu erhalten

Abstract

Introduction

Inflammasome is a multi-protein complex which is an important constituent of innate immunity. It mainly consists of three parts, apoptosis-associated speck-like protein containing caspase recruitment domain (ASC), caspase protease, and a NOD-like receptor (NLR) family protein (such as NLRP1) or an HIN200 family protein (such as AIM2). Inflammasome is widely studied in many autoimmune diseases and chronic inflammatory reactions, such as familial periodic autoinflammatory response, type 2 diabetes, Alzheimer's disease, and atherosclerosis. Activation of inflammasome in the kidney has been widely reported in glomerular and tubular-interstitial diseases. Podocytes play a critical role in maintaining the normal structure and function of glomerular filtration barrier. Recently, it has been demonstrated that podocytes, as a group of renal residential cells, can express all necessary components of NLRP3 inflammasome, which is activated and contribute to inflammatory response in the local kidney.

Methods

Literature review was conducted to further summarize current evidence of podocyte NLRP3 inflammasome activation and related molecular mechanisms under different disease conditions.

Results

Podocytes are a key component of the glomerular filtration barrier, and the loss of podocyte regeneration is a major limiting factor in the recovery of proteinuria. Through a more comprehensive study of inflammasome in podocytes, it will provide new targets and possibilities for the treatment of kidney diseases.

Sharma D, Kanneganti TD. The cell biology of inflammasomes: Mechanisms of inflammasome activation and regulation. J Cell Biol. 2016;213:617–29.PubMedPubMedCentral

Prochnicki T, Latz E. Inflammasomes on the crossroads of innate immune recognition and metabolic control. Cell Metab. 2017;26:71–93.PubMed

Hornung V, Ablasser A, Charrel-Dennis M, Bauernfeind F, Horvath G, Caffrey DR, et al. AIM2 recognizes cytosolic dsDNA and forms a caspase-1-activating inflammasome with ASC. Nature. 2009;458:514–8.PubMedPubMedCentral

Brunette RL, Young JM, Whitley DG, Brodsky IE, Malik HS, Stetson DB. Extensive evolutionary and functional diversity among mammalian AIM2-like receptors. J Exp Med. 2012;209:1969–83.PubMedPubMedCentral

Chae JJ, Cho YH, Lee GS, Cheng J, Liu PP, Feigenbaum L, et al. Gain-of-function Pyrin mutations induce NLRP3 protein-independent interleukin-1beta activation and severe autoinflammation in mice. Immunity. 2011;34:755–68.PubMedPubMedCentral

Xu H, Yang J, Gao W, Li L, Li P, Zhang L, et al. Innate immune sensing of bacterial modifications of Rho GTPases by the Pyrin inflammasome. Nature. 2014;513:237–41.PubMed

Chang A, Ko K, Clark MR. The emerging role of the inflammasome in kidney diseases. Curr Opin Nephrol Hypertens. 2014;23:204–10.PubMedPubMedCentral

Hornung V, Bauernfeind F, Halle A, Samstad EO, Kono H, Rock KL, et al. Silica crystals and aluminum salts activate the NALP3 inflammasome through phagosomal destabilization. Nat Immunol. 2008;9:847–56.PubMedPubMedCentral

Petrilli V, Papin S, Dostert C, Mayor A, Martinon F, Tschopp J. Activation of the NALP3 inflammasome is triggered by low intracellular potassium concentration. Cell Death Differ. 2007;14:1583–9.PubMed

10.

Bauernfeind F, Bartok E, Rieger A, Franchi L, Nunez G, Hornung V. Cutting edge: reactive oxygen species inhibitors block priming, but not activation, of the NLRP3 inflammasome. J Immunol. 2011;187:613–7.PubMedPubMedCentral

11.

Zhou R, Tardivel A, Thorens B, Choi I, Tschopp J. Thioredoxin-interacting protein links oxidative stress to inflammasome activation. Nat Immunol. 2010;11:136–40.PubMed

12.

Zhang C, Boini KM, Xia M, Abais JM, Li X, Liu Q, et al. Activation of Nod-like receptor protein 3 inflammasomes turns on podocyte injury and glomerular sclerosis in hyperhomocysteinemia. Hypertension. 2012;60:154–62.PubMedPubMedCentral

13.

Komada T, Muruve DA. The role of inflammasomes in kidney disease. Nat Rev Nephrol. 2019;15:501–20.PubMed

14.

Juliana C, Fernandes-Alnemri T, Wu J, Datta P, Solorzano L, Yu JW, et al. Anti-inflammatory compounds parthenolide and Bay 11–7082 are direct inhibitors of the inflammasome. J Biol Chem. 2010;285:9792–802.PubMedPubMedCentral

15.

Valino-Rivas L, Gonzalez-Lafuente L, Sanz AB, Ruiz-Ortega M, Ortiz A, Sanchez-Nino MD. Non-canonical NFkappaB activation promotes chemokine expression in podocytes. Sci Rep. 2016;6:28857.PubMedPubMedCentral

16.

Viedt C, Orth SR. Monocyte chemoattractant protein-1 (MCP-1) in the kidney: does it more than simply attract monocytes? Nephrol Dial Transplant. 2002;17:2043–7.PubMed

17.

Zhao Y, Chen SJ, Wang JC, Niu HX, Jia QQ, Chen XW, et al. Sesquiterpene lactones inhibit advanced oxidation protein product-induced MCP-1 expression in podocytes via an IKK/NF-kappaB-dependent mechanism. Oxid Med Cell Longev. 2015;2015:934058.PubMedPubMedCentral

18.

Ridker PM, MacFadyen JG, Glynn RJ, Koenig W, Libby P, Everett BM, et al. Inhibition of Interleukin-1beta by canakinumab and cardiovascular outcomes in patients with chronic kidney disease. J Am Coll Cardiol. 2018;71:2405–14.PubMed

19.

Nowak KL, Chonchol M, Ikizler TA, Farmer-Bailey H, Salas N, Chaudhry R, et al. IL-1 inhibition and vascular function in CKD. J Am Soc Nephrol. 2017;28:971–80.PubMed

20.

Lidar M, Livneh A. Familial mediterranean fever: clinical, molecular and management advancements. Neth J Med. 2007;65:318–24.PubMed

21.

Goldfinger SE. Colchicine for familial Mediterranean fever. N Engl J Med. 1972;287:1302.PubMed

22.

Ozcakar ZB, Ozdel S, Yilmaz S, Kurt-Sukur ED, Ekim M, Yalcinkaya F. Anti-IL-1 treatment in familial Mediterranean fever and related amyloidosis. Clin Rheumatol. 2016;35:441–6.PubMed

23.

Akar S, Cetin P, Kalyoncu U, Karadag O, Sari I, Cinar M, et al. Nationwide experience with off-label use of interleukin-1 targeting treatment in familial mediterranean fever patients. Arthritis Care Res (Hoboken). 2018;70:1090–4.

24.

Sargin G, Kose R, Senturk T. Anti-interleukin-1 treatment among patients with familial Mediterranean fever resistant to colchicine treatment. Retrospect Anal Sao Paulo Med J. 2019;137:39–44.

25.

Zhen J, Zhang L, Pan J, Ma S, Yu X, Li X, et al. AIM2 mediates inflammation-associated renal damage in hepatitis B virus-associated glomerulonephritis by regulating caspase-1, IL-1beta, and IL-18. Mediators Inflamm. 2014;2014:190860.PubMedPubMedCentral

26.

Komada T, Chung H, Lau A, Platnich JM, Beck PL, Benediktsson H, et al. Macrophage uptake of necrotic cell DNA activates the AIM2 inflammasome to regulate a proinflammatory phenotype in CKD. J Am Soc Nephrol. 2018;29:1165–81.PubMedPubMedCentral

27.

Kimkong I, Avihingsanon Y, Hirankarn N. Expression profile of HIN200 in leukocytes and renal biopsy of SLE patients by real-time RT-PCR. Lupus. 2009;18:1066–72.PubMed

28.

Qiu YY, Tang LQ. Roles of the NLRP3 inflammasome in the pathogenesis of diabetic nephropathy. Pharmacol Res. 2016;114:251–64.PubMed

29.

Tsai YL, Hua KF, Chen A, Wei CW, Chen WS, Wu CY, et al. NLRP3 inflammasome: pathogenic role and potential therapeutic target for IgA nephropathy. Sci Rep. 2017;7:41123.PubMedPubMedCentral

30.

Mulay SR, Anders HJ. Crystal nephropathies: mechanisms of crystal-induced kidney injury. Nat Rev Nephrol. 2017;13:226–40.PubMed

31.

Soares JLS, Fernandes FP, Patente TA, Monteiro MB, Parisi MC, Giannella-Neto D, et al. Gain-of-function variants in NLRP1 protect against the development of diabetic kidney disease: NLRP1 inflammasome role in metabolic stress sensing? Clin Immunol. 2018;187:46–9.PubMed

32.

Song F, Ma Y, Bai XY, Chen X. The expression changes of inflammasomes in the aging rat kidneys. J Gerontol A Biol Sci Med Sci. 2016;71:747–56.PubMed

33.

Yuan F, Kolb R, Pandey G, Li W, Sun L, Liu F, et al. Involvement of the NLRC4-inflammasome in diabetic nephropathy. PLoS ONE. 2016;11:e0164135.PubMedPubMedCentral

34.

Russo C, Morabito F, Luise F, Piromalli A, Battaglia L, Vinci A, et al. Hyperhomocysteinemia is associated with cognitive impairment in multiple sclerosis. J Neurol. 2008;255:64–9.PubMed

35.

Ostrakhovitch EA, Tabibzadeh S. Homocysteine in chronic kidney disease. Adv Clin Chem. 2015;72:77–106.PubMed

36.

Xia M, Conley SM, Li G, Li PL, Boini KM. Inhibition of hyperhomocysteinemia-induced inflammasome activation and glomerular sclerosis by NLRP3 gene deletion. Cell Physiol Biochem. 2014;34:829–41.PubMedPubMedCentral

37.

Abais JM, Xia M, Li G, Gehr TW, Boini KM, Li PL. Contribution of endogenously produced reactive oxygen species to the activation of podocyte NLRP3 inflammasomes in hyperhomocysteinemia. Free Radic Biol Med. 2014;67:211–20.PubMed

38.

Abais JM, Zhang C, Xia M, Liu Q, Gehr TW, Boini KM, et al. NADPH oxidase-mediated triggering of inflammasome activation in mouse podocytes and glomeruli during hyperhomocysteinemia. Antioxid Redox Signal. 2013;18:1537–48.PubMedPubMedCentral

39.

Abais JM, Xia M, Li G, Chen Y, Conley SM, Gehr TW, et al. Nod-like receptor protein 3 (NLRP3) inflammasome activation and podocyte injury via thioredoxin-interacting protein (TXNIP) during hyperhomocysteinemia. J Biol Chem. 2014;289:27159–68.PubMedPubMedCentral

40.

Zhang Q, Conley SM, Li G, Yuan X, Li PL. Rac1 GTPase inhibition blocked podocyte injury and glomerular sclerosis during hyperhomocysteinemia via suppression of nucleotide-binding oligomerization domain-like receptor containing pyrin domain 3 inflammasome activation. Kidney Blood Press Res. 2019;44:513–32.PubMed

41.

Li G, Xia M, Abais JM, Boini K, Li PL, Ritter JK. Protective action of anandamide and Its COX-2 metabolite against l-homocysteine-induced NLRP3 inflammasome activation and injury in podocytes. J Pharmacol Exp Ther. 2016;358:61–70.PubMedPubMedCentral

42.

Li G, Chen Z, Bhat OM, Zhang Q, Abais-Battad JM, Conley SM, et al. NLRP3 inflammasome as a novel target for docosahexaenoic acid metabolites to abrogate glomerular injury. J Lipid Res. 2017;58:1080–90.PubMedPubMedCentral

43.

Alicic RZ, Rooney MT, Tuttle KR. Diabetic kidney disease: challenges, progress, and possibilities. Clin J Am Soc Nephrol. 2017;12:2032–45.PubMedPubMedCentral

44.

Gao P, Meng XF, Su H, He FF, Chen S, Tang H, et al. Thioredoxin-interacting protein mediates NALP3 inflammasome activation in podocytes during diabetic nephropathy. Biochim Biophys Acta. 2014;1843:2448–600.PubMed

45.

Shahzad K, Bock F, Dong W, Wang H, Kopf S, Kohli S, et al. Nlrp3-inflammasome activation in non-myeloid-derived cells aggravates diabetic nephropathy. Kidney Int. 2015;87:74–84.PubMed

46.

Liu Q, Zhang L, Zhang W, Hao Q, Qiu W, Wen Y, et al. Inhibition of NF-kappaB reduces renal inflammation and expression of PEPCK in type 2 diabetic mice. Inflammation. 2018;41:2018–29.PubMed

47.

Lei Y, Devarapu SK, Motrapu M, Cohen CD, Lindenmeyer MT, Moll S, et al. Interleukin-1beta Inhibition for chronic kidney disease in obese mice with type 2 diabetes. Front Immunol. 2019;10:1223.PubMedPubMedCentral

48.

Ridker PM, Everett BM, Thuren T, MacFadyen JG, Chang WH, Ballantyne C, et al. Antiinflammatory therapy with canakinumab for atherosclerotic disease. N Engl J Med. 2017;377:1119–31.PubMed

49.

Ridker PM, MacFadyen JG, Thuren T, Everett BM, Libby P, Glynn RJ, et al. Effect of interleukin-1beta inhibition with canakinumab on incident lung cancer in patients with atherosclerosis: exploratory results from a randomised, double-blind, placebo-controlled trial. Lancet. 2017;390:1833–42.PubMed

50.

Ridker PM, Howard CP, Walter V, Everett B, Libby P, Hensen J, et al. Effects of interleukin-1beta inhibition with canakinumab on hemoglobin A1c, lipids, C-reactive protein, interleukin-6, and fibrinogen: a phase IIb randomized, placebo-controlled trial. Circulation. 2012;126:2739–48.PubMed

51.

Choudhury RP, Birks JS, Mani V, Biasiolli L, Robson MD, L'Allier PL, et al. Arterial effects of canakinumab in patients with atherosclerosis and type 2 diabetes or glucose intolerance. J Am Coll Cardiol. 2016;68:1769–80.PubMedPubMedCentral

52.

Gao P, He FF, Tang H, Lei CT, Chen S, Meng XF, et al. NADPH oxidase-induced NALP3 inflammasome activation is driven by thioredoxin-interacting protein which contributes to podocyte injury in hyperglycemia. J Diabetes Res. 2015;2015:504761.PubMedPubMedCentral

53.

Liu Y, Xu Z, Ma F, Jia Y, Wang G. Knockdown of TLR4 attenuates high glucose-induced podocyte injury via the NALP3/ASC/Caspase-1 signaling pathway. Biomed Pharmacother. 2018;107:1393–401.PubMed

54.

Yu Q, Zhang M, Qian L, Wen D, Wu G. Luteolin attenuates high glucose-induced podocyte injury via suppressing NLRP3 inflammasome pathway. Life Sci. 2019;225:1–7.PubMed

55.

Chertow GM, Hsu CY, Johansen KL. The enlarging body of evidence: obesity and chronic kidney disease. J Am Soc Nephrol. 2006;17:1501–2.PubMed

56.

de Vries AP, Ruggenenti P, Ruan XZ, Praga M, Cruzado JM, Bajema IM, et al. Fatty kidney: emerging role of ectopic lipid in obesity-related renal disease. Lancet Diabetes Endocrinol. 2014;2:417–26.PubMed

57.

Boini KM, Xia M, Koka S, Gehr TW, Li PL. Instigation of NLRP3 inflammasome activation and glomerular injury in mice on the high fat diet: role of acid sphingomyelinase gene. Oncotarget. 2016;7:19031–44.PubMedPubMedCentral

58.

Boini KM, Xia M, Abais JM, Li G, Pitzer AL, Gehr TW, et al. Activation of inflammasomes in podocyte injury of mice on the high fat diet: Effects of ASC gene deletion and silencing. Biochim Biophys Acta. 2014;1843:836–45.PubMedPubMedCentral

59.

Hou XX, Dong HR, Sun LJ, Yang M, Cheng H, Chen YP. Purinergic 2X7 receptor is involved in the podocyte damage of obesity-related glomerulopathy via activating nucleotide-binding and oligomerization domain-like receptor protein 3 inflammasome. Chin Med J (Engl). 2018;131:2713–25.

60.

Solini A, Menini S, Rossi C, Ricci C, Santini E, Blasetti Fantauzzi C, et al. The purinergic 2X7 receptor participates in renal inflammation and injury induced by high-fat diet: possible role of NLRP3 inflammasome activation. J Pathol. 2013;231:342–53.PubMed

61.

Wang W, Ding XQ, Gu TT, Song L, Li JM, Xue QC, et al. Pterostilbene and allopurinol reduce fructose-induced podocyte oxidative stress and inflammation via microRNA-377. Free Radic Biol Med. 2015;83:214–26.PubMed

62.

Zhao J, Rui HL, Yang M, Sun LJ, Dong HR, Cheng H. CD36-mediated lipid accumulation and activation of NLRP3 inflammasome lead to podocyte injury in obesity-related glomerulopathy. Mediators Inflamm. 2019;2019:3172647.PubMedPubMedCentral

63.

Ren Y, Wang D, Lu F, Zou X, Xu L, Wang K, et al. Coptidis Rhizoma inhibits NLRP3 inflammasome activation and alleviates renal damage in early obesity-related glomerulopathy. Phytomedicine. 2018;49:52–655.PubMed

64.

Hu C, Rusin CG, Tan Z, Guagliardo NA, Barrett PQ. Zona glomerulosa cells of the mouse adrenal cortex are intrinsic electrical oscillators. J Clin Invest. 2012;122:2046–53.PubMedPubMedCentral

65.

Blasi ER, Rocha R, Rudolph AE, Blomme EA, Polly ML, McMahon EG. Aldosterone/salt induces renal inflammation and fibrosis in hypertensive rats. Kidney Int. 2003;63:1791–800.PubMed

66.

Chen D, Chen Z, Park C, Centrella M, McCarthy T, Chen L, et al. Aldosterone stimulates fibronectin synthesis in renal fibroblasts through mineralocorticoid receptor-dependent and independent mechanisms. Gene. 2013;531:23–30.PubMed

67.

Wang B, Ding W, Zhang M, Li H, Gu Y. Rapamycin attenuates aldosterone-induced tubulointerstitial inflammation and fibrosis. Cell Physiol Biochem. 2015;35:116–25.PubMed

68.

Bai M, Chen Y, Zhao M, Zhang Y, He JC, Huang S, et al. NLRP3 inflammasome activation contributes to aldosterone-induced podocyte injury. Am J Physiol Renal Physiol. 2017;312:F556–F564.PubMed

69.

Zhao M, Bai M, Ding G, Zhang Y, Huang S, Jia Z, et al. Angiotensin II Stimulates the NLRP3 Inflammasome to Induce Podocyte Injury and Mitochondrial Dysfunction. Kidney Dis (Basel). 2018;4:83–94.

70.

Lee CK, Son SH, Park KK, Park JH, Lim SS, Chung WY. Isoliquiritigenin inhibits tumor growth and protects the kidney and liver against chemotherapy-induced toxicity in a mouse xenograft model of colon carcinoma. J Pharmacol Sci. 2008;106:444–51.PubMed

71.

Wang Z, Wang N, Han S, Wang D, Mo S, Yu L, et al. Dietary compound isoliquiritigenin inhibits breast cancer neoangiogenesis via VEGF/VEGFR-2 signaling pathway. PLoS One. 2013;8:e68566.PubMedPubMedCentral

72.

Kakegawa H, Matsumoto H, Satoh T. Inhibitory effects of some natural products on the activation of hyaluronidase and their anti-allergic actions. Chem Pharm Bull (Tokyo). 1992;40:1439–42.

73.

Tawata M, Aida K, Noguchi T, Ozaki Y, Kume S, Sasaki H, et al. Anti-platelet action of isoliquiritigenin, an aldose reductase inhibitor in licorice. Eur J Pharmacol. 1992;212:87–92.PubMed

74.

Honda H, Nagai Y, Matsunaga T, Okamoto N, Watanabe Y, Tsuneyama K, et al. Isoliquiritigenin is a potent inhibitor of NLRP3 inflammasome activation and diet-induced adipose tissue inflammation. J Leukoc Biol. 2014;96:1087–100.PubMed

75.

Xiong D, Hu W, Ye ST, Tan YS. Isoliquiritigenin alleviated the Ang II-induced hypertensive renal injury through suppressing inflammation cytokines and oxidative stress-induced apoptosis via Nrf2 and NF-kappaB pathways. Biochem Biophys Res Commun. 2018;506:161–8.PubMed

76.

Patricia Moreno-Londono A, Bello-Alvarez C, Pedraza-Chaverri J. Isoliquiritigenin pretreatment attenuates cisplatin induced proximal tubular cells (LLC-PK1) death and enhances the toxicity induced by this drug in bladder cancer T24 cell line. Food Chem Toxicol. 2017;109:143–54.PubMed

77.

Tang Y, Wang C, Wang Y, Zhang J, Wang F, Li L, et al. Isoliquiritigenin attenuates LPS-induced AKI by suppression of inflammation involving NF-kappaB pathway. Am J Transl Res. 2018;10:4141–51.PubMedPubMedCentral

78.

Kriz W. Podocyte is the major culprit accounting for the progression of chronic renal disease. Microsc Res Tech. 2002;57:189–95.PubMed

79.

Xiong J, Wang Y, Shao N, Gao P, Tang H, Su H, et al. The Expression and significance of NLRP3 inflammasome in patients with primary glomerular diseases. Kidney Blood Press Res. 2015;40:344–54.PubMed

80.

Yan J, Li Y, Yang H, Zhang L, Yang B, Wang M, et al. Interleukin-17A participates in podocyte injury by inducing IL-1beta secretion through ROS-NLRP3 inflammasome-caspase-1 pathway. Scand J Immunol. 2018;87:e12645.PubMed

81.

Yang X, Wu Y, Li Q, Zhang G, Wang M, Yang H, et al. CD36 Promotes podocyte apoptosis by activating the pyrin domain-containing-3 (NLRP3) inflammasome in primary nephrotic syndrome. Med Sci Monit. 2018;24:6832–9.PubMedPubMedCentral

82.

Wang Y, Yu F, Song D, Wang SX, Zhao MH. Podocyte involvement in lupus nephritis based on the 2003 ISN/RPS system: a large cohort study from a single centre. Rheumatol (Oxf). 2014;53:1235–44.

83.

Fu R, Guo C, Wang S, Huang Y, Jin O, Hu H, et al. Podocyte Activation of NLRP3 inflammasomes contributes to the development of proteinuria in lupus nephritis. Arthritis Rheumatol. 2017;69:1636–46.PubMedPubMedCentral

84.

Fu R, Xia Y, Li M, Mao R, Guo C, Zhou M, et al. Pim-1 as a therapeutic target in lupus nephritis. Arthritis Rheumatol. 2019;71:1308–18.PubMed

85.

Guo C, Fu R, Zhou M, Wang S, Huang Y, Hu H, et al. Pathogenesis of lupus nephritis: RIP3 dependent necroptosis and NLRP3 inflammasome activation. J Autoimmun. 2019;103:102286.PubMed

86.

Wali RK, Drachenberg CI, Papadimitriou JC, Keay S, Ramos E. HIV-1-associated nephropathy and response to highly-active antiretroviral therapy. Lancet. 1998;352:783–4.PubMed

87.

Haque S, Lan X, Wen H, Lederman R, Chawla A, Attia M, et al. HIV promotes NLRP3 inflammasome complex activation in murine HIV-associated nephropathy. Am J Pathol. 2016;186:347–58.PubMedPubMedCentral

88.

Anders HJ. Immune system modulation of kidney regeneration–mechanisms and implications. Nat Rev Nephrol. 2014;10:347–58.PubMed

89.

Swanson KV, Deng M, Ting JP. The NLRP3 inflammasome: molecular activation and regulation to therapeutics. Nat Rev Immunol. 2019;19:477–89.PubMed

90.

Zhang G, Li Q, Wang L, Chen Y, Wang L, Zhang W. Interleukin-1beta enhances the intracellular accumulation of cholesterol by up-regulating the expression of low-density lipoprotein receptor and 3-hydroxy-3-methylglutaryl coenzyme A reductase in podocytes. Mol Cell Biochem. 2011;346:197–204.PubMed

91.

Lamkanfi M. Emerging inflammasome effector mechanisms. Nat Rev Immunol. 2011;11:213–20.PubMed

Titel: Inflammasome activation in podocytes: a new mechanism of glomerular diseases
verfasst von: Wei Xiong
Xian-Fang Meng
Chun Zhang
Publikationsdatum: 24.05.2020
Verlag: Springer International Publishing
Erschienen in: Inflammation Research / Ausgabe 8/2020
Print ISSN: 1023-3830
Elektronische ISSN: 1420-908X
DOI: https://doi.org/10.1007/s00011-020-01354-w

Leitlinien kompakt für die Innere Medizin

Mit medbee Pocketcards sicher entscheiden.

^{Seit 2022 gehört die medbee GmbH zum Springer Medizin Verlag}

Kostenlos registrieren

Neu im Fachgebiet Innere Medizin

Positiver FIT: Die Ursache liegt nicht immer im Dickdarm

27.05.2024 Blut im Stuhl Nachrichten

Immunchemischer Stuhltest positiv, Koloskopie negativ – in solchen Fällen kann die Blutungsquelle auch weiter proximal sitzen. Ein Forschungsteam hat nachgesehen, wie häufig und in welchen Lokalisationen das der Fall ist.

GLP-1-Agonisten können Fortschreiten diabetischer Retinopathie begünstigen

24.05.2024 Diabetische Retinopathie Nachrichten

Möglicherweise hängt es von der Art der Diabetesmedikamente ab, wie hoch das Risiko der Betroffenen ist, dass sich sehkraftgefährdende Komplikationen verschlimmern.

Mehr Lebenszeit mit Abemaciclib bei fortgeschrittenem Brustkrebs?

24.05.2024 Mammakarzinom Nachrichten

In der MONARCHE-3-Studie lebten Frauen mit fortgeschrittenem Hormonrezeptor-positivem, HER2-negativem Brustkrebs länger, wenn sie zusätzlich zu einem nicht steroidalen Aromatasehemmer mit Abemaciclib behandelt wurden; allerdings verfehlte der numerische Zugewinn die statistische Signifikanz.

ADT zur Radiatio nach Prostatektomie: Wenn, dann wohl länger

24.05.2024 Prostatakarzinom Nachrichten

Welchen Nutzen es trägt, wenn die Strahlentherapie nach radikaler Prostatektomie um eine Androgendeprivation ergänzt wird, hat die RADICALS-HD-Studie untersucht. Nun liegen die Ergebnisse vor. Sie sprechen für länger dauernden Hormonentzug.

Update Innere Medizin

Bestellen Sie unseren Fach-Newsletter und bleiben Sie gut informiert.

Newsletter bestellen

Live-Webinar "Urologie und Sexualmedizin in der Praxis"

Springer Medizin

Abstract

Introduction

Methods

Results

Bitte loggen Sie sich ein, um Zugang zu diesem Inhalt zu erhalten

Weitere Artikel der Ausgabe 8/2020

Fertility and infertility implications in rheumatoid arthritis; state of the art

Immunoglobulin free light chains: an inflammatory biomarker of diabetes

The unleashing of the immune system in COVID-19 and sepsis: the calm before the storm?

The protective effects of phoenixin-14 against lipopolysaccharide-induced inflammation and inflammasome activation in astrocytes

TMEM88 modulates the secretion of inflammatory factors by regulating YAP signaling pathway in alcoholic liver disease