Role of the β
Acute kidney injury
Formoterol
β2-adrenergic receptor
Journal
Pharmacological reports : PR
ISSN: 2299-5684
Titre abrégé: Pharmacol Rep
Pays: Switzerland
ID NLM: 101234999
Informations de publication
Date de publication:
26 Apr 2024
26 Apr 2024
Historique:
received:
07
12
2023
accepted:
03
04
2024
revised:
28
03
2024
medline:
26
4
2024
pubmed:
26
4
2024
entrez:
26
4
2024
Statut:
aheadofprint
Résumé
Podocytes have a remarkable ability to recover from injury; however, little is known about the recovery mechanisms involved in this process. We recently showed that formoterol, a long-acting β We genetically deleted the β A similar level of injury was observed in β These results indicate that the podocyte β
Sections du résumé
BACKGROUND
BACKGROUND
Podocytes have a remarkable ability to recover from injury; however, little is known about the recovery mechanisms involved in this process. We recently showed that formoterol, a long-acting β
METHODS
METHODS
We genetically deleted the β
RESULTS
RESULTS
A similar level of injury was observed in β
CONCLUSIONS
CONCLUSIONS
These results indicate that the podocyte β
Identifiants
pubmed: 38668812
doi: 10.1007/s43440-024-00594-5
pii: 10.1007/s43440-024-00594-5
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : NIDDK NIH HHS
ID : R01DK087956
Pays : United States
Organisme : NIDDK NIH HHS
ID : R56DK116887
Pays : United States
Organisme : NIDDK NIH HHS
ID : P30DK074038
Pays : United States
Organisme : NIGMS NIH HHS
ID : GM084147
Pays : United States
Informations de copyright
© 2024. The Author(s).
Références
Reiser J, Altintas MM. Podocytes. F1000Res. 2016;5:114.
doi: 10.12688/f1000research.7255.1
Haraldsson B, Nystrom J, Deen WM. Properties of the glomerular barrier and mechanisms of proteinuria. Physiol Rev. 2008;88(2):451–87.
doi: 10.1152/physrev.00055.2006
pubmed: 18391170
Brinkkoetter PT, Ising C, Benzing T. The role of the podocyte in albumin filtration. Nat Rev Nephrol. 2013;9(6):328–36.
doi: 10.1038/nrneph.2013.78
pubmed: 23609563
Lal MA, Patrakka J. Understanding podocyte biology to develop novel kidney therapeutics. Front Endocrinol. 2018;9:409.
doi: 10.3389/fendo.2018.00409
Torban E, Braun F, Wanner N, Takano T, Goodyer PR, Lennon R, et al. From podocyte biology to novel cures for glomerular disease. Kidney Int. 2019;96(4):850–61.
doi: 10.1016/j.kint.2019.05.015
pubmed: 31420194
Durvasula RV, Shankland SJ. Podocyte injury and targeting therapy: an update. Curr Opin Nephrol Hypertens. 2006;15(1):1–7.
doi: 10.1097/01.mnh.0000199012.79670.0b
pubmed: 16340659
Bhargava P, Janda J, Schnellmann RG. Elucidation of cGMP-dependent induction of mitochondrial biogenesis through PKG and p38 MAPK in the kidney. Am J Physiol Renal Physiol. 2020;318(2):F322–8.
doi: 10.1152/ajprenal.00533.2019
pubmed: 31841384
Arif E, Nihalani D. Beta2-adrenergic receptor in kidney biology: a current prospective. Nephrology. 2019;24(5):497–503.
doi: 10.1111/nep.13584
pubmed: 30848004
Cameron RB, Gibbs WS, Miller SR, Dupre TV, Megyesi J, Beeson CC, et al. Proximal tubule beta 2-adrenergic receptor mediates formoterol-induced recovery of mitochondrial and renal function after ischemia-reperfusion injury. J Pharmacol Exp Ther. 2019;369(1):173–80.
doi: 10.1124/jpet.118.252833
pubmed: 30709866
Johnstone DB, Zhang JZ, George B, Leon C, Gachet C, Wong H, et al. Podocyte-specific deletion of Myh9 encoding nonmuscle myosin heavy chain 2A predisposes mice to glomerulopathy. Mol Cell Biol. 2011;31(10):2162–70.
doi: 10.1128/MCB.05234-11
pubmed: 21402784
pmcid: 3133349
Hizawa N. Pharmacogenetics of beta2-agonists. Allergol Int. 2011;60(3):239–46.
doi: 10.2332/allergolint.11-RAI-0317
pubmed: 21681016
Syamsu, Yusuf I, Patellongi I. The effect of polymorphism of the beta-2 adrenergic receptor on the response to beta-2 agonist in bronchial asthma patients. Acta Med Indones. 2007;39(1):8–12.
pubmed: 17297203
Johnson M. Molecular mechanisms of beta(2)-adrenergic receptor function, response, and regulation. J Allergy Clin Immunol. 2006;117(1):18–24.
doi: 10.1016/j.jaci.2005.11.012
pubmed: 16387578
Wachter SB, Gilbert EM. Beta-adrenergic receptors, from their discovery and characterization through their manipulation to beneficial clinical application. Cardiology. 2012;122(2):104–12.
doi: 10.1159/000339271
pubmed: 22759389
Arif E, Solanki AK, Srivastava P, Rahman B, Fitzgibbon WR, Deng P, et al. Mitochondrial biogenesis induced by the beta2-adrenergic receptor agonist formoterol accelerates podocyte recovery from glomerular injury. Kidney Int. 2019;96(3):656–73.
doi: 10.1016/j.kint.2019.03.023
pubmed: 31262488
pmcid: 6708766
Solanki AK, Srivasta P, Rahman B, Lipschutz JH, Nihalani D, Arif E. The Use of high-throughput transcriptomics to identify pathways with therapeutic significance in podocytes. Int J Mol Sci. 2020;21(1):274.
doi: 10.3390/ijms21010274
Hinoi E, Gao N, Jung DY, Yadav V, Yoshizawa T, Meyers MG, et al. The sympathetic tone mediates leptin’s inhibition of insulin secretion by modulating osteocalcin bioactivity. J Cell Biol. 2008;183(7):1235–42.
doi: 10.1083/jcb.200809113
pubmed: 19103808
pmcid: 2606962
Scholpa NE, Simmons EC, Tilley DG, Schnellmann RG. Beta2-adrenergic receptor-mediated mitochondrial biogenesis improves skeletal muscle recovery following spinal cord injury. Exp Neurol. 2019;322: 113064.
doi: 10.1016/j.expneurol.2019.113064
pubmed: 31525347
pmcid: 7751764
Velez JCQ, Arif E, Rodgers J, Hicks MP, Arthur JM, Nihalani D, et al. Deficiency of the angiotensinase aminopeptidase A increases susceptibility to glomerular injury. J Am Soc Nephrol. 2017;28(7):2119–32.
doi: 10.1681/ASN.2016111166
pubmed: 28202497
pmcid: 5491295
Verma R, Kovari I, Soofi A, Nihalani D, Patrie K, Holzman LB. Nephrin ectodomain engagement results in Src kinase activation, nephrin phosphorylation, Nck recruitment, and actin polymerization. J Clin Invest. 2006;116(5):1346–59.
doi: 10.1172/JCI27414
pubmed: 16543952
pmcid: 1401486
Arif E, Rathore YS, Kumari B, Ashish F, Wong HN, Holzman LB, et al. Slit diaphragm protein Neph1 and its signaling: a novel therapeutic target for protection of podocytes against glomerular injury. J Biol Chem. 2014;289(14):9502–18.
doi: 10.1074/jbc.M113.505743
pubmed: 24554715
pmcid: 3975002
Sagar A, Arif E, Solanki AK, Srivastava P, Janech MG, Kim SH, et al. Targeting Neph1 and ZO-1 protein-protein interaction in podocytes prevents podocyte injury and preserves glomerular filtration function. Sci Rep. 2017;7(1):12047.
doi: 10.1038/s41598-017-12134-8
pubmed: 28935902
pmcid: 5608913
Masszi A, Fan LF, Rosivall L, McCulloch CA, Rotstein OD, Muscsi I, et al. Integrity of cell-cell contacts is a critical regulator of TGF-beta 1-induced epithelial-to-myofibroblast transition: role for beta-catenin. Am J Pathol. 2004;165(6):1955–67.
doi: 10.1016/S0002-9440(10)63247-6
pubmed: 15579439
pmcid: 1618715
Ng YY, Huang TP, Yang WC, Chen ZP, Yang AH, Mu W, et al. Tubular epithelial-myofibroblast transdifferentiation in progressive tubulointerstitial fibrosis in 5/6 nephrectomized rats. Kidney Int. 1998;54(3):864–76.
doi: 10.1046/j.1523-1755.1998.00076.x
pubmed: 9734611
Lopes TG, Souza ML, Silva VD, Santos MD, Silva WIC, Itaquy TP, et al. Markers of renal fibrosis: how do they correlate with podocyte damage in glomerular diseases? PLoS ONE. 2019;14(6): e0217585.
doi: 10.1371/journal.pone.0217585
pubmed: 31220088
pmcid: 6586273
Muller-Deile J, Schiffer M. Podocytes from the diagnostic and therapeutic point of view. Pflugers Arch. 2017;469(7–8):1007–15.
doi: 10.1007/s00424-017-1993-z
pubmed: 28508947
Faul C, Connelly M, Merscher-Gomez S, Chang YH, Franz S, Delfgaauw J, et al. The actin cytoskeleton of kidney podocytes is a direct target of the antiproteinuric effect of cyclosporine A. Nat Med. 2008;14(9):931–8.
doi: 10.1038/nm.1857
pubmed: 18724379
pmcid: 4109287
Shankland SJ, Eitner F, Hudkins KL, Goodpaster T, D’Agati V, Alpers CE. Differential expression of cyclin-dependent kinase inhibitors in human glomerular disease: role in podocyte proliferation and maturation. Kidney Int. 2000;58(2):674–83.
doi: 10.1046/j.1523-1755.2000.00213.x
pubmed: 10916090
Fukuda A, Wickman LT, Venkatareddy MP, Sato Y, Chowdhury MA, Wang SQ, et al. Angiotensin II-dependent persistent podocyte loss from destabilized glomeruli causes progression of end stage kidney disease. Kidney Int. 2012;81(1):40–55.
doi: 10.1038/ki.2011.306
pubmed: 21937979