ライフサイエンスコーパス: podocyte

1 anti-PLA2R autoantibodies which bind to the podocyte.

2 e salutary effects of glucocorticoids in the podocyte.

3 ve depletion of all VEGF-A isoforms from the podocytes.

4 min-induced ER stress and apoptosis in human podocytes.

5 analysis confirmed that ShcA is expressed in podocytes.

6 red conditionally immortalized human and rat podocytes.

7 b mediates radiation-induced damage of renal podocytes.

8 with the palmitic acid-induced autophagy in podocytes.

9 aused increased intracellular Ca(2+) flux in podocytes.

10 N1A might be a key regulator of ER stress in podocytes.

11 ed signaling via PKC in kidney cells such as podocytes.

12 r 1 and protease-activated receptor 4 in rat podocytes.

13 ructure and improves cell survival in murine podocytes.

14 nd protease-activated receptor 4 in cultured podocytes.

15 rylation of focal adhesion kinase and AKT in podocytes.

16 ated downregulation of WT1(-KTS) isoforms in podocytes.

17 n, mitophagy, and deformed foot processes in podocytes.

18 ype of ordinarily quiescent adult glomerular podocytes.

19 sion levels of claudin-1 mRNA and protein in podocytes.

20 d by MYH9(+/E1841K) then MYH9(E1841K/E1841K) podocytes.

21 6) channels in cardiomyocytes and glomerular podocytes.

22 ificantly increased PLK2 expression in mouse podocytes.

23 nnel activity and cytoskeletal remodeling in podocytes.

24 ed gene, Bax, and Bax/Bcl2 ratio in cultured podocytes.

25 hat palmitic acid (PA) promoted autophagy in podocytes.

26 confer a radioprotective effect in cultured podocytes.

27 as found leading to an enhanced ER stress in podocytes.

28 ing GN through proinflammatory activation of podocytes.

29 ecialized glomerular epithelial cells called podocytes.

30 ulfenylation in mouse glomeruli and cultured podocytes.

31 signaling opponent of other PKC isoforms in podocytes.

32 and impaired migration compared to wild type podocytes.

33 c kidney and in high glucose-induced damaged podocytes.

34 -transactivated and -transrepressed genes in podocytes.

35 8 mitogen-activated protein kinase (MAPK) in podocytes.

36 UBAM complex in albumin endocytosis in human podocytes.

37 SGS pathogenesis in the absence of a primary podocyte abnormality.

38 Supernatants from ABIN1[D472N] podocytes accelerated chemotaxis of human neutrophils, a

39 ar claudin-1, is markedly upregulated in the podocyte, accompanied by a tighter filtration slit and t

40 Within the podocyte, all three proteins were enriched in the plasma

41 However, in the absence of intrinsic podocyte alterations, the origin of the pathogenic signa

42 on and decreased the migration rate of human podocytes, an established intermediate phenotype of SRNS

43 resence of endothelial damage, and disrupted podocyte and endothelial integrity in 6 week-old Cd2ap-K

44 Podocyte and glomerular research is center stage for the

45 y histological changes, but also ameliorated podocyte and glomeruli injury in diabetic mice, which we

46 s gene is essential for zebrafish pronephric podocyte and proximal tubular function and that the ctns

47 d3 and UTX increased the H3K27me3 content of podocytes and attenuated glomerular disease in adriamyci

48 G or PPAR-gamma enhanced TRPC6 expression in podocytes and counteracted effects of sildenafil and 8-B

49 inally, the level of KLF15 expression in the podocytes and glomeruli from human biopsy specimens corr

50 ex offers insights into the role of PLA2R in podocytes and how autoantibodies might disrupt PLA2R fun

51 al (4-HNE), a marker of oxidative stress, in podocytes and increased the phosphorylation of AKT2, an

52 ased the mitochondrial membrane potential in podocytes and induced podocyte apoptosis, while the inhi

53 orescence revealed SGPL1 expression in mouse podocytes and mesangial cells.

54 iants has also been shown to cause injury to podocytes and other cell types, but the underlying mecha

55 -X-C chemokine receptor 7, was documented on podocytes and PECs, respectively.

56 Patient podocytes and RPE cells carrying disease-associated CFH

57 grin beta3 signaling pathway in human kidney podocytes and smooth muscle cells.

58 oduction of reactive oxygen species (ROS) in podocytes and that NAC (N-acetyl-cysteine), a potent ant

59 sed both mRNA and protein levels of SIRT1 in podocytes and that puerarin led to SIRT1-mediated deacet

60 nding of the function of the cytoskeleton in podocytes and the associated implications for pathophysi

61 is essential in maintaining the integrity of podocytes and the glomerular filtration barrier of the k

62 highlight the homeostatic actions of JAK2 in podocytes and the importance of TFEB to autophagosome-ly

63 peptidase A (APA) is expressed in glomerular podocytes and tubular epithelia and metabolizes angioten

64 e obtained 3-D electron microscopy images of podocytes and used quantitative features to build dynami

65 transmembrane glycoproteins expressed by the podocyte, and both induce IgG4-predominant humoral immun

66 3 and protease-activated receptor 4 in human podocytes, and between protease-activated receptor 1 and

67 promoter region of the Notch ligand Jag1 in podocytes, and derepression of Jag1 by EZH2 inhibition o

68 472N] (D485N homolog) cultured human-derived podocytes, and interaction with primary human neutrophil

69 eins encoded by these genes are expressed in podocytes, and malfunction of these proteins leads to a

70 toantibodies against the recently discovered podocyte antigens: the M-type phospholipase A2 receptor

71 d that silencing PLK2 attenuates HDG-induced podocyte apoptosis and inflammation, which may serve as

72 membrane potential in podocytes and induced podocyte apoptosis, while the inhibition of autophagy by

73 However, it was still unclear whether podocytes are able to migrate during acute injury.

74 Podocytes are becoming a primary focus of research effor

75 We demonstrated that human podocytes are committed to performing endocytosis via a

76 the treatment of proteinuric kidney disease.Podocytes are essential components of the renal glomerul

77 Podocytes are glomerular epithelial cells that are norma

78 Podocytes are increasingly recognized as key players in

79 This in vivo study reveals that podocytes are very stationary cells making regenerative

80 Podocytes, as an important component of the filtration b

81 interferon beta, and RANTES in ZIKV-infected podocytes at 72 hours, compared with renal GECs and mesa

82 excretion that was accompanied by increased podocyte autophagosome fractional volume and p62 aggrega

83 nhibition had a direct, protective effect on podocyte barrier function.

84 is intact and that Gc induced an increase in podocyte barrier function.

85 ling pathways involved in stiffness-mediated podocyte behaviors are identified, revealing the interde

86 o-differentiation and maturation response in podocytes better than substrates either softer or stiffe

87 Until now, the question if podocytes can be replaced by immigration of cells along

88 Loss of podocytes can occur as a result of excessive intracellul

89 ction of claudin-1 gene expression in mature podocytes caused profound proteinuria, and with deep-etc

90 The loss of podocytes causes proteinuria, which is involved in the p

91 lities in Col4a3 mutants including distorted podocyte cell bodies and disorganized primary processes.

92 nt filamentous microprojections arising from podocyte cell bodies and processes, and presence of uniq

93 et of miR-92a that constitutively safeguards podocyte cell cycle quiescence.

94 h a cDNA expression library developed from a podocyte cell line derived from a child with HIVAN led t

95 In this study, using human podocyte cell lines overexpressing either myc-LMX1BWT or

96 This scarring is due to loss of podocytes, cells critical for glomerular filtration, and

97 lammatory mediators in ABIN1[D472N] cultured podocytes compared with WT cells.

98 Held April 3-6, 2016, the 11th International Podocyte Conference took place in Haifa and Jerusalem, I

99 Ultrastructural examination of podocytes confirmed more robust foot process effacement

100 beta-catenin overexpression in PKC-deficient podocytes could restore the wild-type phenotype, similar

101 ith podocyte function, which is observed for podocytes cultured on gelatin-mTG gels of physiological

102 monstrate that even slight impairment of the podocyte cytoskeletal apparatus results in proteinuria a

103 BM could represent a trigger of both further podocyte cytoskeletal changes and inflammation, thereby

104 benefit kidney filter dynamics by balancing podocyte cytoskeletal remodeling.

105 shown to interact with nephrin and regulate podocyte cytoskeleton and slit diaphragm dynamics, MAGI2

106 s-level evidence that the slit diaphragm and podocyte cytoskeleton are regulated targets of proteolyt

107 vitro also occurred in two in vivo models of podocyte damage (WT1 heterozygous knockout mice and puro

108 n 43 and purinergic signaling contributes to podocyte damage in GN.

109 ation of preferential protease motifs during podocyte damage indicated activation of caspase protease

110 inflammatory and fibrotic responses, driving podocyte damage through downstream activation of integri

111 teolytic modification, which is altered upon podocyte damage.

112 -L1(-) PMN in GN development and in inducing podocyte damage.

113 ch ultimately leads to inflammatory-mediated podocyte death and glomerular scarring.

114 of the histone methylating enzyme EZH2 from podocytes decreased H3K27me3 levels and sensitized mice

115 by EZH2 inhibition or knockdown facilitated podocyte dedifferentiation.

116 Yet, when exposed to LPS, GR knockout podocytes demonstrated fewer stress fibers and impaired

117 Morphologically, irradiated podocytes demonstrated loss of filopodia and remodeling

118 Dysregulation of RPE- and podocyte-derived VEGF is associated with neovascularizat

119 in characterizing the mechanisms involved in podocyte development, metabolism, acquired injury, and r

120 podocytes, we could show that the remaining podocytes did not walk along GBM during 24 h.

121 7aa, in zebrafish larvae resulted in altered podocyte differentiation and impaired glomerular filtrat

122 that treatment with glucocorticoids restores podocyte differentiation markers and normal ultrastructu

123 nscription factor, is required for restoring podocyte differentiation markers in mice and human podoc

124 taxis of human neutrophils, and ABIN1[D472N] podocytes displayed a greater susceptibility to injuriou

125 activation and integration of HIV-1 into the podocyte DNA.

126 the renal glomerular filtration barrier and podocyte dysfunction leads to proteinuric kidney disease

127 we investigated whether PLK2 contributes to podocyte dysfunction, a characteristic change in the dev

128 stant nephrotic syndrome is characterized by podocyte dysfunction.

129 Visualizing the glomerular endothelium and podocyte-endothelium interface revealed the presence of

130 Podocytes exhibit a unique cytoskeletal architecture tha

131 Mice in which JAK2 had been deleted from podocytes exhibited an elevation in urine albumin excret

132 ytometry immunophenotyping revealed that rat podocytes express the protease-activated receptor family

133 nephrosis, and suggest that thrombin and/or podocyte-expressed thrombin receptors may be novel thera

134 p2 expression in murine kidneys and cultured podocytes following an LPS challenge.

135 ; severe albuminuria, nephrinuria, FSGS, and podocyte foot effacement in Ang II-induced hypertension;

136 ceptor expression, which is a key factor for podocyte foot process effacement and proteinuria.

137 These mice were protected from acute podocyte foot process effacement following protamine sul

138 a complex filtration apparatus consisting of podocyte foot processes, glomerular basement membrane an

139 Here Liu et al. show that Sirt6 protects podocytes from apoptosis and inflammation by increasing

140 In vitro, isolated primary podocytes from MYH9(E1841K/E1841K) mice exhibited increa

141 efore radiation exposure partially protected podocytes from SMPDL3b loss, cytoskeletal remodeling, an

142 gene and protein expression associated with podocyte function, which is observed for podocytes cultu

143 effects of the mutation on the expression of podocyte genes such as NPHS1, GLEPP1, and WT1.

144 rm ratio and a decrease in the expression of podocyte genes.

145 We conclude that the podocyte glucocorticoid receptor is important for limiti

146 ina densa tend to accumulate upstream of the podocyte glycocalyx that spans the slit, but none are ob

147 ion into the lamina densa of the GBM and the podocyte glycocalyx, together with saturable tubular cap

148 uced by either LPS or nephrotoxic serum, the podocyte GR knockout mice demonstrated worsened proteinu

149 rimary podocytes isolated from wild type and podocyte GR knockout mice showed similar actin stress fi

150 Interestingly, SMPDL3b-overexpressing podocytes had higher basal levels of sphingosine-1-phosp

151 Pkm-knockdown immortalized mouse podocytes had higher levels of toxic glucose metabolites

152 Wound healing assays revealed that MYH9(+/+) podocytes had the lowest migration rate, followed by MYH

153 Podocytes have a unique 3D structure of major and interd

154 dicating its significant role in maintaining podocyte health.

155 ticoid receptor (GR) in the nucleus of human podocytes (HPCs), a key cell type in the glomerulus crit

156 Furthermore, C1-Ten causes podocyte hypertrophy and proteinuria by increasing mTORC

157 butes to the pathogenesis of DKD by inducing podocyte hypertrophy under high glucose conditions.

158 mTORC1 hyperactivation leads to podocyte hypertrophy, but the detailed mechanism of how

159 ice, consistent with an altered phenotype of podocytes in culture.

160 ypertrophy is a prominent feature of damaged podocytes in diabetic kidney disease (DKD).

161 Podocytes in glomeruli from humans with focal segmental

162 mber of the mannose receptor family found in podocytes in human kidney.

163 uerarin exerts the anti-oxidative effects in podocytes in the diabetic milieu.

164 asing evidence points to the central role of podocytes in the pathogenesis.

165 To study how steroids directly affect the podocytes in the treatment of proteinuria, we created a

166 In this study, we found that human podocytes in vitro are committed to internalizing albumi

167 Treatment of podocytes in vitro with TGF-beta1 resulted in increased

168 Sirt6 has pleiotropic protective actions in podocytes, including anti-inflammatory and anti-apoptoti

169 induced significant morphological changes in podocytes, including disruption of the actin cytoskeleta

170 the direct effects of glucocorticoids on the podocyte, independent of the immunomodulatory effects, m

171 ent staining of glomerular epithelial cells (podocytes) indicated that VtE ameliorates podocyte patho

172 mutations and increased TRPC6 expression in podocytes induce glomerular injury and proteinuria.

173 phrocytes, fly cells homologous to mammalian podocytes, induced increased endocytic activity and accu

174 id-like 3B (SMPDL3b) is a key determinant of podocyte injury and a known off target of the anti-CD20

175 n excretion with marked mesangial expansion, podocyte injury and apoptosis, but without blood pressur

176 termined the roles of RTN1A and ER stress in podocyte injury and DN.

177 Thus, sildenafil ameliorates podocyte injury and prevents proteinuria through cGMP- a

178 ession in vitro In a rat model of reversible podocyte injury and proteinuria, phosphorylated nephrin

179 -dependent mechanisms, thereby counteracting podocyte injury and proteinuria.

180 Identifying the molecular mechanisms of podocyte injury and survival is important for better und

181 a implicate thrombinuria as a contributor to podocyte injury during nephrosis, and suggest that throm

182 potential therapeutic targets for preventing podocyte injury has clinical importance.

183 us hypothesized that thrombin contributes to podocyte injury in a protease-activated receptor-specifi

184 suggest that ER stress plays a major role in podocyte injury in DN and RTN1A might be a key regulator

185 rated perturbation of protease action during podocyte injury in vitro, including diminished proteolys

186 Podocyte injury is a major determinant of proteinuric ki

187 Podocyte injury is an early event in diabetic kidney dis

188 Podocyte injury is the inciting event in primary glomeru

189 dvances, the signaling pathways that mediate podocyte injury remain poorly understood.

190 t histone deacetylase Sirt6 protects against podocyte injury through epigenetic regulation of Notch s

191 roreductase/metronidazole zebrafish model of podocyte injury to in vivo two-photon microscopy.

192 The mechanistic role of HbF in podocyte injury was studied in pregnant rabbits.

193 nary albumin excretion, segmental sclerosis, podocyte injury, and apoptosis.

194 versed age-related increases in proteinuria, podocyte injury, fibronectin accumulation, TGF-beta expr

195 e proteins leads to a universal end point of podocyte injury, glomerular filtration barrier disruptio

196 n of ABIN1 function exacerbated proteinuria, podocyte injury, glomerular NF-kappaB activity, glomerul

197 pioglitazone dose-dependently downregulated podocyte injury-induced TRPC6 expression in vitro Knockd

198 role in other model systems, KIBRA promotes podocyte injury.

199 tant for limiting proteinuria in settings of podocyte injury.

200 er thrombin concentrations may contribute to podocyte injury.

201 osclerosis, characterized by proteinuria and podocyte injury.

202 otecting against diabetic glomerulopathy and podocyte injury.

203 However, NP/GC-A/cGMP signaling protects podocyte integrity under pathologic conditions, most lik

204 functional role of the TJ in the glomerular podocyte is unclear.

205 ependent stimulation of Ca(2+) influx in the podocytes is precluded by blocking either AT1 or AT2 rec

206 However, its role in podocytes is unclear.

207 Primary podocytes isolated from wild type and podocyte GR knocko

208 In immortalized mouse podocytes, JAK2 knockdown decreased TFEB promoter activi

209 In cultured podocytes, knockdown of JAK2 similarly impaired autophag

210 lk between glomerular endothelial injury and podocytes leads to defects and depletion, albuminuria, a

211 deletion accentuated albuminuria with severe podocyte lesions and recruitment of pathogenic parietal

212 Drosophila garland cell nephrocytes are podocyte-like cells and thus provide a potential in vivo

213 Notably, LPAR inhibition slowed podocyte loss (podocytes per glomerulus +/-SEM at 8 week

214 icroscopy studies demonstrated prevention of podocyte loss and structural alterations, the absence of

215 ameliorates podocyte pathology and prevents podocyte loss in the DGKalpha(+/+) mice but not in the D

216 iorated diabetes-induced endothelial injury, podocyte loss, albuminuria, and glomerulosclerosis.

217 mutations resulted in lack of or diminished podocyte MAGI2 expression.

218 ibronectin and type IV collagen, and loss of podocyte markers WT1 and synaptopodin, as determined by

219 identified, revealing the interdependence of podocyte mechanotransduction and maintenance of their ph

220 We conclude that podocyte morphology, optimized for filtration, is intrin

221 gII content and attenuated the expression of podocyte nephrin in APA-KO mice but not in wild-type con

222 but had no effect on mesangial expansion or podocyte numbers.

223 Pals1 expression in renal tubular cells and podocytes of human kidneys.

224 e that microRNA-92a (miR-92a) is enriched in podocytes of patients and mice with RPGN.

225 RTN1A and ER stress marker expression in the podocytes of TUDCA-treated mice.

226 d in urinary extracellular vesicles (EVs) of podocyte origin and accompanied by increased urinary sol

227 bbits increased the number of urinary EVs of podocyte origin.

228 embling those observed in cultured mammalian podocytes overexpressing APOL1-G1.

229 s (podocytes) indicated that VtE ameliorates podocyte pathology and prevents podocyte loss in the DGK

230 claudins and the TJ have essential roles in podocyte pathophysiology and that claudin interactions w

231 tably, LPAR inhibition slowed podocyte loss (podocytes per glomerulus +/-SEM at 8 weeks: 667+/-40, n=

232 derlies the beneficial effect of Bis-T-23 on podocyte physiology.

233 ultured with human endothelial cells (EC) or podocytes (PO).

234 icroprojections were observed extending from podocyte processes and cell body, indicating significant

235 KIBRA/WWc1 overexpression in murine podocytes promoted LATS kinase phosphorylation, leading

236 e reflective of preeclampsia-related altered podocyte protein expression.

237 mini to comprehensively characterize cleaved podocyte proteins in the glomerulus in vivo We found evi

238 results in various proteoforms of important podocyte proteins, including those of podocin, nephrin,

239 I infected primary human podocytes, renal glomerular endothelial cells (GECs), an

240 Kidney podocytes represent a key constituent of the glomerular

241 presented their work on new developments in podocyte research.

242 ls, the retinal pigment epithelium (RPE) and podocytes, respectively.

243 ly, overexpression of TFEB in JAK2-deficient podocytes reversed lysosomal dysfunction and restored al

244 demonstrating the role of ang II in inducing podocyte SDF-1 production, which ultimately activates PE

245 n which kidney damage is caused not by local podocyte-selective injury but more likely by systemic in

246 The cytoskeleton regulates podocyte shape, structure, stability, slit diaphragm ins

247 Drosophila nephrocytes and human podocytes share striking similarities, but to what degre

248 seased glomeruli, we demonstrate that kidney podocytes show marked stiffness sensitivity.

249 Moreover, the protective effects of podocyte Shp2 deficiency were associated with decreased

250 To determine the role of podocyte Shp2 in vivo, we generated podocyte-specific Sh

251 Nephrin is a key structural component of the podocyte slit diaphragm, and proper expression of nephri

252 e glomerular basement membrane is thickened, podocyte slit width is increased and sub-podocyte space

253 increase in glomerular basement membrane and podocyte slit width, as well as the decrease in sub-podo

254 ed, podocyte slit width is increased and sub-podocyte space coverage is reduced when VEGF-A is deplet

255 e slit width, as well as the decrease in sub-podocyte space coverage, produced by VEGF-A depletion.

256 tide and p38 MAPK in podocytes, we generated podocyte-specific (pod) GC-A conditional KO (cKO) mice.

257 Podocyte-specific deletion of miR-92a in mice de-repress

258 f proteinuria, we created a mouse model with podocyte-specific deletion of the glucocorticoid recepto

259 The podocyte-specific glucocorticoid receptor (GR) knockout

260 Here we generated mice with podocyte-specific inducible expression of the APOL1 refe

261 f NPs on podocytes, we generated mice with a podocyte-specific knockout of GC-A (Podo-GC-A KO).

262 osis models, and thrombin colocalized with a podocyte-specific marker in rat glomeruli.

263 Podocyte-specific markers that are critical in the forma

264 Podocyte-specific Pkm2-knockout (KO) mice with diabetes

265 increased podocyte TRPC6 expression, as did podocyte-specific PPAR-gamma knockout mice, which were m

266 Renal histologic expression of the podocyte-specific protein, nephrin, but not podocin, is

267 sses associated with a reduced expression of podocyte-specific proteins and a formation of subpodocyt

268 ry EVs containing immunologically detectable podocyte-specific proteins by digital flow cytometry and

269 We hypothesized that renal expression of podocyte-specific proteins would be reflected in urinary

270 role of podocyte Shp2 in vivo, we generated podocyte-specific Shp2 knockout (pod-Shp2 KO) mice.

271 copy vividly demonstrated the restoration of podocyte structure by SS-31.

272 markers, restored glomerular capillaries and podocyte structure, and arrested glomerulosclerosis and

273 of ErbB4/EGFR with erlotinib co-treatment of podocytes suppressed this signaling.

274 glomerular filtration barrier that promotes podocyte survival by inhibiting dendrin pro-apoptotic fu

275 that sildenafil inhibits TRPC6 expression in podocytes through PPAR-gamma-dependent mechanisms, there

276 the hypothesis that Gc acts directly on the podocyte to produce clinically useful effects without in

277 the marked reduction of GC-A mRNA in GC-A KO podocytes to 1% of the control level, Podo-GC-A KO mice

278 Exposing human podocytes to albumin overload prompted an increase in CU

279 Moreover, treatment of podocytes to inhibit endocytic transport or dynamin acti

280 The ability of podocytes to secrete vesicles containing PLA2R provides

281 The loss of podocytes triggers a focal activation of parietal epithe

282 agonists displayed proteinuria and increased podocyte TRPC6 expression, as did podocyte-specific PPAR

283 While podocytes typically de-differentiate in culture and show

284 te differentiation markers in mice and human podocytes under cell stress.

285 yrosine phosphorylation has been observed in podocytes under pathological conditions, but the molecul

286 An exception is in RPGN where podocytes undergo a deregulation of their differentiated

287 onary cells making regenerative processes by podocyte walking along the GBM very unlikely.

288 By 4D in vivo observation of single podocytes, we could show that the remaining podocytes di

289 In human podocytes, we demonstrated that the basic GR-signalling

290 To study the effects of NPs on podocytes, we generated mice with a podocyte-specific kn

291 ction of natriuretic peptide and p38 MAPK in podocytes, we generated podocyte-specific (pod) GC-A con

292 KIBRA knockdown podocytes were also protected against protamine-induced

293 In contrast, SMPDL3b overexpressing podocytes were protected from radiation-induced cytoskel

294 Here, we show that treating cultured mouse podocytes with Bis-T-23 promoted stress fiber formation

295 Treatment of cultured podocytes with connexin 43-specific blocking peptides at

296 e recapitulated in differentiated E11 murine podocytes with lentiviral-mediated Shp2 knockdown.

297 Microarrays of proximal tubular cells and podocytes with stable HIF1alpha and/or HIF2alpha suppres

298 new mechanism for Gc action directly on the podocyte, with translational relevance to designing new

299 ction destabilized the SD protein complex in podocytes, with significantly reduced expression and alt

300 lar epithelial cells, endothelial cells, and podocytes, working in concert.