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000180319 0247_ $$2doi$$a10.1016/j.cmet.2022.04.009
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000180319 041__ $$aEnglish
000180319 082__ $$a570
000180319 1001_ $$aGarreta, Elena$$b0
000180319 245__ $$aA diabetic milieu increases ACE2 expression and cellular susceptibility to SARS-CoV-2 infections in human kidney organoids and patient cells.
000180319 260__ $$aCambridge, Mass.$$bCell Press$$c2022
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000180319 520__ $$aIt is not well understood why diabetic individuals are more prone to develop severe COVID-19. To this, we here established a human kidney organoid model promoting early hallmarks of diabetic kidney disease development. Upon SARS-CoV-2 infection, diabetic-like kidney organoids exhibited higher viral loads compared with their control counterparts. Genetic deletion of the angiotensin-converting enzyme 2 (ACE2) in kidney organoids under control or diabetic-like conditions prevented viral detection. Moreover, cells isolated from kidney biopsies from diabetic patients exhibited altered mitochondrial respiration and enhanced glycolysis, resulting in higher SARS-CoV-2 infections compared with non-diabetic cells. Conversely, the exposure of patient cells to dichloroacetate (DCA), an inhibitor of aerobic glycolysis, resulted in reduced SARS-CoV-2 infections. Our results provide insights into the identification of diabetic-induced metabolic programming in the kidney as a critical event increasing SARS-CoV-2 infection susceptibility, opening the door to the identification of new interventions in COVID-19 pathogenesis targeting energy metabolism.
000180319 536__ $$0G:(DE-HGF)POF4-316$$a316 - Infektionen, Entzündung und Krebs (POF4-316)$$cPOF4-316$$fPOF IV$$x0
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000180319 650_7 $$2Other$$aACE2
000180319 650_7 $$2Other$$aCOVID-19
000180319 650_7 $$2Other$$aSARS-CoV-2
000180319 650_7 $$2Other$$aangiotensin-converting enzyme 2
000180319 650_7 $$2Other$$adiabetes 2
000180319 650_7 $$2Other$$ahuman kidney organoids
000180319 650_7 $$0EC 3.4.15.1$$2NLM Chemicals$$aPeptidyl-Dipeptidase A
000180319 650_7 $$0EC 3.4.17.23$$2NLM Chemicals$$aAngiotensin-Converting Enzyme 2
000180319 650_2 $$2MeSH$$aAngiotensin-Converting Enzyme 2
000180319 650_2 $$2MeSH$$aCOVID-19
000180319 650_2 $$2MeSH$$aDiabetes Mellitus
000180319 650_2 $$2MeSH$$aDiabetic Nephropathies
000180319 650_2 $$2MeSH$$aHumans
000180319 650_2 $$2MeSH$$aKidney: metabolism
000180319 650_2 $$2MeSH$$aOrganoids
000180319 650_2 $$2MeSH$$aPeptidyl-Dipeptidase A: genetics
000180319 650_2 $$2MeSH$$aPeptidyl-Dipeptidase A: metabolism
000180319 650_2 $$2MeSH$$aSARS-CoV-2
000180319 7001_ $$aPrado, Patricia$$b1
000180319 7001_ $$0P:(DE-He78)8c3dd76230733f354d346a2fbe8db355$$aStanifer, Megan L$$b2$$udkfz
000180319 7001_ $$aMonteil, Vanessa$$b3
000180319 7001_ $$aMarco, Andrés$$b4
000180319 7001_ $$aUllate-Agote, Asier$$b5
000180319 7001_ $$aMoya-Rull, Daniel$$b6
000180319 7001_ $$aVilas-Zornoza, Amaia$$b7
000180319 7001_ $$aTarantino, Carolina$$b8
000180319 7001_ $$aRomero, Juan Pablo$$b9
000180319 7001_ $$aJonsson, Gustav$$b10
000180319 7001_ $$aOria, Roger$$b11
000180319 7001_ $$aLeopoldi, Alexandra$$b12
000180319 7001_ $$aHagelkruys, Astrid$$b13
000180319 7001_ $$aGallo, Maria$$b14
000180319 7001_ $$aGonzález, Federico$$b15
000180319 7001_ $$aDomingo-Pedrol, Pere$$b16
000180319 7001_ $$aGavaldà, Aleix$$b17
000180319 7001_ $$aDel Pozo, Carmen Hurtado$$b18
000180319 7001_ $$aHasan Ali, Omar$$b19
000180319 7001_ $$aVentura-Aguiar, Pedro$$b20
000180319 7001_ $$aCampistol, Josep María$$b21
000180319 7001_ $$aProsper, Felipe$$b22
000180319 7001_ $$aMirazimi, Ali$$b23
000180319 7001_ $$0P:(DE-He78)4658b59d5b4e54b919fc63ab1213c78f$$aBoulant, Steeve$$b24$$udkfz
000180319 7001_ $$aPenninger, Josef M$$b25
000180319 7001_ $$aMontserrat, Nuria$$b26
000180319 773__ $$0PERI:(DE-600)2174469-5$$a10.1016/j.cmet.2022.04.009$$gVol. 34, no. 6, p. 857 - 873.e9$$n6$$p857 - 873.e9$$tCell metabolism$$v34$$x1550-4131$$y2022
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