Biomedical subjects

Feng Zheng

Publications and source records attributed to Feng Zheng.

At least 19 recordsLinked to original sources

PubMed2026

Efficacy and safety of ferric citrate tablets in Chinese patients with hyperphosphatemia undergoing maintenance hemodialysis: a multicenter, randomized, open-label, active-controlled, phase III trial.

BACKGROUND: This study aimed to evaluate the efficacy and safety of ferric citrate tablets in Chinese patients with hyperphosphatemia undergoing maintenance hemodialysis (MHD). METHODS: In this phase III, multicenter, randomized, open-label, non-inferiority trial, patients with hyperphosphatemia on maintenance hemodialysis were randomly assigned to receive either ferric citrate or sevelamer carbonate tablets for 12 weeks. The primary endpoint was the change in serum phosphorus levels from baseline to week 12, with a non-inferiority margin of 0.32 mmol/L. Secondary endpoints included changes in serum calcium, intact parathyroid hormone, and safety assessments. RESULTS: A total of 239 patients were randomized to the ferric citrate group (n = 119) or the sevelamer carbonate group (n = 120). The mean change in serum phosphorus levels was -0.70 ± 0.50 mmol/L in the ferric citrate group and -0.61 ± 0.59 mmol/L in the sevelamer carbonate group (least squares mean difference, -0.09 mmol/L; 95% CI, -0.24 to 0.05 mmol/L; non-inferiority margin, 0.32 mmol/L). No significant inter-group differences were found in the percentage of patients achieving target phosphorus levels (49.09% vs. 48.28%, p = 0.902). Ferric citrate significantly improved iron-related parameters and hemoglobin levels. Most treatment-emergent adverse events were mild, with gastrointestinal disorders being the most common. CONCLUSIONS: Ferric citrate tablets were non-inferior to sevelamer carbonate in reducing serum phosphorus levels in hyperphosphatemia patients on maintenance hemodialysis, with the added benefit of improving iron-related anemia and a favorable safety profile.

Adult↗

PubMed2025

Multi-omics analyses provide insights into the molecular basis for salt tolerance of Phyla nodiflora.

The perennial herbaceous plant, Phyla nodiflora (Verbenaceae), which possesses natural resistance to multiple abiotic stresses, is widely used as a pioneer species in island ecological restoration. Due to the lack of information about its genome, the mechanism underlying its tolerance to environmental stresses, such as salinity, is almost entirely unknown. Here, we report on the high-quality genome of P. nodiflora that is 403.07 Mb in size, and which was assembled and anchored onto 18 pseudo-chromosomes. Genomic synteny revealed that P. nodiflora underwent two whole genome duplication events, which promoted the expansion of genes related to environmental adaptation and the biosynthesis of secondary metabolites. An integrated genomic and transcriptomic analysis suggested that salt stress tolerance in P. nodiflora is associated with the expansion and activated expression of genes related to abscisic acid (ABA) homeostasis and signaling. The expansion of ZEP family genes may contribute to the consistent increase in ABA levels under salt stress. Lysine acetylomic analysis revealed that exposure to salt led to widespread protein deacetylation, with these proteins primarily involved in signal transduction, carbohydrate transport and metabolism, and transcription regulation. Deacetylation of glutathione S-transferase increased enzymatic activities in response to salt-induced oxidative stress. Collectively, the genomic, transcriptomic, and lysine acetylomic analyses provide profound insight into the molecular basis of the adaptation of P. nodiflora to salt stress, and will be helpful to engineer salt-tolerant plants for ecological restoration.

Salt Tolerance↗

PubMed2006

Synthesis of L-beta-3'-deoxy-3',3'-difluoro-4'-thionucleosides.

[Structure: see text] An efficient route to L-beta-3'-deoxy-3',3'-difluoro-4'-thionucleosides, thio-containing analogues of highly bioactive gemcitabine, is described. Our synthesis highlighted the installation of the thioacetyl group in high efficiency and construction of 3-deoxy-3,3-difluorothiofuranose skeleton in a novel method.

Models, Molecular↗

PubMed2006

Diagnosis of colorectal cancer using Raman spectroscopy of laser-trapped single living epithelial cells.

A single-cell diagnostic technique for epithelial cancers is developed by utilizing laser trapping and Raman spectroscopy to differentiate cancerous and normal epithelial cells. Single-cell suspensions were prepared from surgically removed human colorectal tissues following standard primary culture protocols and examined in a near-infrared laser-trapping Raman spectroscopy system, where living epithelial cells were investigated one by one. A diagnostic model was built on the spectral data obtained from 8 patients and validated by the data from 2 new patients. Our technique has potential applications from epithelial cancer diagnosis to the study of cell dynamics of carcinogenesis.

Adenocarcinoma↗

PubMed2006

Single-walled carbon nanotube paper as a sorbent for organic vapor preconcentration.

Single-walled carbon nanotubes were examined as an adsorptive material for a thermally desorbed preconcentrator for organic vapors. The nanotubes were processed into a paper form and packed into a metal tube for flow-through sampling. Adsorbed vapors were released by a temperature-programmed desorption method and detected downstream with a flexural plate wave vapor sensor. The tested vapors, methyl ethyl ketone, toluene, and dimethyl methylphosphonate, were released from the packed column at different temperatures. The vapors were retained more strongly than previously observed for the widely used Tenax porous polymer, indicating a significant affinity of the single walled nanotubes for organic vapors.

Journal Article↗

PubMed2006

IRF-8/interferon (IFN) consensus sequence-binding protein is involved in Toll-like receptor (TLR) signaling and contributes to the cross-talk between TLR and IFN-gamma signaling pathways.

Toll-like receptor (TLR) and interferon-gamma (IFN-gamma) signaling pathways are important for both innate and adaptive immune responses. However, the cross-talk between these two signaling pathways is incompletely understood. Here we show that IFN-gamma and LPS synergistically induce the expression of proinflammatory factors, including interleukin-1 (IL-1), IL-6, IL-12, NO, and tumor necrosis factor-alpha (TNF-alpha). Comparable synergism was observed between IFN-gamma and peptidoglycan (PGN; a TLR2 ligand) and poly(I:C) (a TLR3 ligand) in the induction of IL-12 promoter activity. IFN-gamma enhanced lipopolysaccharide (LPS)-induced ERK and JNK phosphorylation but had no effect on LPS-induced NF-kappaB activation. Interestingly, we found that IRF-8-/- macrophages were impaired in the activation of LPS-induced ERK and JNK and the production of proinflammatory cytokines induced by LPS or IFN-gamma plus LPS. Retroviral transduction of IRF-8 into IRF-8-/- macrophages rescued ERK and JNK activation. Furthermore, co-immunoprecipitation experiments show that IRF-8 physically interacts with TRAF6 at a binding site between amino acid residues 356 and 305 of IRF-8. Transfection of IRF-8 enhanced TRAF6 ubiquitination, which is consistent with a physical interaction of IRF-8 with TRAF6. Taken together, the results suggest that the interaction of IRF-8 with TRAF6 modulates TLR signaling and may contribute to the cross-talk between IFN-gamma and TLR signal pathways.

Cell Line↗

PubMed2006

Determination of BAPTA-AM, the acetoxymethyl tetraester of BAPTA, in rat plasma by liquid chromatography tandem mass spectrometry.

BAPTA-AM is the acetoxymethylester of the calcium chelator BAPTA and has demonstrated efficacy in several animal models of cerebral ischemia. This paper describes the development of a method for the determination of BAPTA-AM in rat plasma by liquid chromatography/tandem mass spectrometry. Owing to multiple ester groups in the structure of BAPTA-AM, [M + Na](+) was chosen as the analytical ion for quantification of BAPTA-AM. During the analytical method development, a high percentage of organic solvent and the addition of an amount of sodium acetate and formic acid in the mobile phase were found to favor the sensitivity and reproducibility of [M + Na](+). Poor fragmentation was usually observed in the MS/MS spectra of sodium adduct ions. However, abundant and reproducible fragment ions were observed for the BAPTA-AM sodium adduct ion, and therefore the traditional selective reaction-monitoring mode was used to further improve the sensitivity of MS detection. Because of the lability of the ester bond, a combination of fluoride and hydrochloric acid was applied to minimize the enzymatic hydrolysis, and acetonitrile was chosen to avoid the chemical hydrolysis or solvolysis during the sample collection and preparation procedure. On the basis of these studies, a rapid, sensitive and reproducible method for the determination of BAPTA-AM in rat plasma, using LC/ESI-MS/MS and a simple protein precipitation procedure, was developed and validated. Also, the present method was successfully applied to the determination of BAPTA-AM plasma concentrations for pharmacokinetic studies in rats.

Animals↗

PubMed2006

Stem cells and kidney injury.

PURPOSE OF REVIEW: The most commonly used therapies in nephrology target the reduction of acute injury, reduction of the rate of progression, or renal replacement therapy. The purpose of this review is to examine new evidence that renal progenitors can be used for therapeutic purposes. Stem cells possess two characteristics, self-renewal and the capacity for multilineage differentiation. They are typically classified as derived from embryos or from the adult. RECENT FINDINGS: New studies on embryonic stem cells show that they can be use to enrich for specific renal progenitors, which integrate into mature structures. Studies on adult stem cells show that almost all kidney cell types can be renewed by adult stem cells originating in bone marrow. Moreover, some animal studies demonstrate that a phenotype such as the aging and diabetic phenotype can be transferred from progenitors residing in the bone marrow, suggesting that the bone marrow contains renal progenitors that may be useful for therapeutic purposes. SUMMARY: Stem cell therapy opens the door to regenerative nephrology. Embryonic stem cells are a useful tool to determine the pathways to convert a pluripotent stem cell into renal progenitors. Adult stem cells in the bone marrow or in a specific kidney niche may provide a source of stem cells with a therapeutic potential.

Animals↗

PubMed2006

Reduced acute vascular injury and atherosclerosis in hyperlipidemic mice transgenic for lysozyme.

Hyperlipidemia promotes oxidant stress, inflammation, and atherogenesis in apolipoprotein E-deficient (ApoE((-/-))) mice. Mice transgenic for lysozyme (LZ-Tg) are resistant to acute and chronic oxidative stress and have decreased circulating levels of pro-oxidant advanced glycation end-products (AGEs). Herein we report that TIB-186 macrophages transduced with adenovirus-expressing human LZ (AdV-LZ) containing the AGE-binding domain facilitated AGE uptake and degradation and that AdV-LZ-transduced macrophages and peritoneal macrophages from LZ-Tg mice suppressed the AGE-triggered tumor necrosis factor-alpha response. We assessed atherosclerosis in LZ-Tg mice crossed with ApoE((-/-)) mice (LZ/ApoE((-/-))) and found increased serum LZ levels and decreased AGE and 8-isoprostanes levels, although hyperlipidemia remained similar to ApoE((-/-)) controls. Atherosclerotic plaques and neointimal lesions at the aortic root and descending aorta were markedly decreased (by 40% and 80%, respectively) in LZ/ApoE((-/-)) versus ApoE((-/-)) mice, as were inflammatory infiltrates. The arterial lesions following femoral artery injury in LZ/ApoE((-/-)) mice were suppressed (intimal to media ratio decreased by 50%), as were AGE deposits and vascular smooth muscle cell activation, compared to ApoE((-/-)) mice. Despite hyperlipidemia, development of atheroma and occlusive, inflammatory arterial neointimal lesions in response to injury was suppressed in LZ/ApoE((-/-)) mice. This effect may be due to the antioxidant properties of LZ, which is possibly linked to the AGE-binding domain region of the molecule.

Adenoviridae↗

PubMed2006

[Comparative study on three types of digestive reconstruction after total gastrectomy].

OBJECTIVE: To investigate the rational digestive reconstruction after total gastrectomy for gastric malignancy. METHODS: Three types of digestive reconstruction were performed after total gastrectomy in 189 cases with gastric carcinoma. The operating time, morbidity and mortality, food intake, digestive tract symptoms, nutritional status at 1 and 3 years after surgery and 1-, 3-, 5-year cumulative survival were compared. RESULTS: There were no significant differences among the three procedures in operative morbidity and mortality, postoperative food intake, nutritional status (Hemoglobin, total protein and labium), and incidences of diarrhea and dumping syndrome (P > 0.05). The overall 1-, 3-, 5-year survival rates were 75.3%, 38.2% and 20.5% respectively, and there were no significant differences among the three groups (P > 0.05). Orr-type and P-type esophagojejunostomy had an advantage of anti-esophageal reflux, and were obviously superior to Moynihan-type anastomosis (P< 0.01). Compared with P-type reconstruction, Orr-type reconstruction was simpler with shorter operating time, and less complications. CONCLUSIONS: Orr-type Roux-en-Y esophagojejunostomy can be recommended as an adaptable method of digestive reconstruction after total gastrectomy for gastric cancer because of its avoiding reflux esophagitis, maintaining better nutritional status and quality of life, and simpler procedure.

Adult↗

PubMed2005

Amelioration of oxidant stress by the defensin lysozyme.

Reactive oxidant species (ROS), products of normal metabolism, cause oxidant injury if they accumulate in pathological amounts. Lysozyme (LZ) contains an 18-amino acid domain that binds agents such as advanced glycation end products (AGE) that generate ROS. We examined whether endogenous LZ affected physiological, or baseline, antioxidant balance and provided protection against both acute and chronic oxidant injury, using paraquat and H2O2 as agents of acute injury and AGE for chronic injury. Hen egg LZ-Tg mice had threefold higher serum LZ levels and decreased baseline AGE levels in serum and liver. These findings were linked to an enhanced baseline systemic GSH-to-GSSG ratio. Baseline levels of stress response genes p66(Shc) and c-Jun were also lower in liver tissue of LZ-Tg mice. Survival from severe oxidant injury induced by paraquat was twofold greater in LZ-Tg mice. In addition, LZ-Tg mice were resistant to chronic exogenous oxidant stress (OS) induced by AGE administration. Preincubation of hepatocytes (Hep G2) with LZ suppressed redox balance at baseline, as well as OS after added paraquat, AGE, or H2O2. LZ also ameliorated paraquat-enhanced cell apoptosis in a dose-dependent manner and suppressed AGE-induced p66(Shc) expression and c-Jun phosphorylation in Hep G2 cells. Thus LZ provides protection against acute and chronic oxidant injury by mechanisms involving suppression of ROS generation and of OS response genes.

Adaptor Proteins, Signal Transducing↗

PubMed2005

Effect of tissue plasminogen activator on vascular smooth muscle cells.

OBJECTIVE: Engineered overexpression of tissue plasminogen activator (tPA) in vascular cells has been proposed as a means to decrease intravascular thrombosis; however, tPA gene transfer has augmented intimal hyperplasia in vivo in some studies. The purpose of this study was to define in vitro the effect of tPA gene transfer on smooth muscle cells (SMCs). METHODS: Human SMCs were retrovirally transduced with the tPA gene (SMCs/tPA). RESULTS: In the absence of plasminogen, no statistical differences in proliferation, migration, and morphology were observed between SMCs/tPA and SMCs. In the presence of plasminogen, many differences became apparent. Matrix metalloproteinase-2 (MMP-2) activation was 10-fold higher in SMCs/tPA than in SMCs. This activation was inhibited by aprotinin, a plasmin inhibitor. Collagen degradation increased sevenfold in SMCs/tPA. SMCs/tPA contracted dramatically in the presence of plasminogen. This cell contraction, indicative of extracellular matrix degradation, was blocked by aprotinin and partially inhibited by MMP inhibitors. SMC/tPA-conditioned medium induced significantly more SMC proliferation. The migration of SMCs/tPA through a porous membrane significantly exceeded untransduced SMCs. CONCLUSIONS: Over-expression of tPA in SMCs results in increased extracellular matrix degradation and can promote cell proliferation and migration. This effect is mediated via plasmin, which further activates MMP-2. CLINICAL RELEVANCE: TPA has been clinically used as a thrombolytic agent in the treatment of acute thrombotic disorders. Transferring the tPA gene into vascular cells as a strategy of gene therapy has been proposed to enhance fibrinolytic capability and therefore inhibit thrombosis and restenosis after vascular interventions. The mechanism(s) by which tPA affects SMC proliferation and vascular remodeling has not been thoroughly characterized. This study unveils the relationship between thrombolytic activity and intimal hyperplasia by showing how the elevated expression of tPA affects the vascular remodeling. This study underscores that the overexpression of an enzyme thought beneficial to blood flow can potentially compromise blood flow by altering the biology of the cell engineered to express it. The results are important to the rational engineering of bioactive grafts with better patency. A new strategy to enhance the thrombolytic ability of a vascular surface without inducing excessive neointimal hyperplasia is proposed.

Analysis of Variance↗

PubMed2005

Insulin resistance and type 2 diabetes in high-fat-fed mice are linked to high glycotoxin intake.

Dietary advanced glycosylation end products (AGEs) have been linked to insulin resistance in db/db(++) mice. To test whether dietary AGEs play a role in the progression of insulin resistance in normal mice fed high-fat diets, normal C57/BL6 mice were randomly assigned to high-fat diets (35% g fat), either high (HAGE-HF group; 995.4 units/mg AGE) or low (by 2.4-fold LAGE-HF group; 329.6 units/mg AGE) in AGE content for 6 months. Age-matched C57/BL6 and db/db(++) mice fed regular diet (5% g fat, 117.4 units/mg AGE) served as controls. After 6 months, 75% of HAGE-HF mice were diabetic and exhibited higher body weight (P < 0.001), fasting glucose (P < 0.001), insulin (P < 0.001), and serum AGEs (P < 0.01) than control mice, while none of the LAGE-HF mice were diabetic despite a similar rise in body weight and plasma lipids. The HAGE-HF group displayed markedly impaired glucose and insulin responses during glucose tolerance tests and euglycemic and hyperglycemic clamps and altered pancreatic islet structure and function compared with those of LAGE-HF mice, in which findings resembled those of control mice. The HAGE-HF group had more visceral fat (by two- and fourfold) and more AGE-modified fat (by two- and fivefold) than LAGE-HF and control mice, respectively. In the HAGE-HF group, plasma 8-isoprostane was higher (P < 0.01) and adiponectin lower (P < 0.001) than control mice, while in the LAGE-HF group, these were more modestly affected (P < 0.05). These results demonstrate that the development of insulin resistance and type 2 diabetes during prolonged high-fat feeding are linked to the excess AGEs/advanced lipoxidation end products inherent in fatty diets.

Adiponectin↗

PubMed2004

Novel lipoglycopeptides as inhibitors of bacterial signal peptidase I.

Signal peptidase (SPase) I is responsible for the cleavage of signal peptides of many secreted proteins in bacteria. Because of its unique physiological and biochemical properties, it serves as a potential target for development of novel antibacterial agents. In this study, we report the production, isolation, and structure determination of a family of structurally related novel lipoglycopeptides from a Streptomyces sp. as inhibitors of SPase I. Detailed spectroscopic analyses, including MS and NMR, revealed that these lipoglycopeptides share a common 14-membered cyclic peptide core, an acyclic tripeptide chain, and a deoxy-alpha-mannose sugar, but differ in the degree of oxidation of the N-methylphenylglycine residue and the length and branching of the fatty acyl chain. Biochemical analysis demonstrated that these peptides are potent and competitive inhibitors of SPase I with K(i) 50 to 158 nm. In addition, they showed modest antibacterial activity against a panel of pathogenic Gram-positive and Gram-negative bacteria with minimal inhibitory concentration of 8-64 microm against Streptococcus pneumonniae and 4-8 microm against Escherichia coli. Notably, they mechanistically blocked the protein secretion in whole cells as demonstrated by inhibiting beta-lactamase release from Staphylococcus aureus. Taken together, the present discovery of a family of novel lipoglycopeptides as potent inhibitors of bacterial SPase I may lead to the development of a novel class of broad-spectrum antibiotics.

Binding, Competitive↗

PubMed2004

The glomerulosclerosis of aging in females: contribution of the proinflammatory mesangial cell phenotype to macrophage infiltration.

Age-associated renal changes may be an important cause of renal failure. We recently found that aged female B6 mice developed progressive glomerular lesions. This was associated with macrophage infiltration, a frequent finding in glomerulosclerosis. We used these mice as a model for studying the mechanisms of glomerular aging. We compared the gene expression profile of intact glomeruli from late postmenopausal (28-month-old) mice to that of intact glomeruli from premenopausal (5-month-old) mice. We found that inflammation-related genes, especially those expressed by activated macrophages, were up-regulated in the glomeruli of 28-month-old mice, a result correlating with the histological observation of glomerular macrophage infiltration. The mechanism for macrophage recruitment could have been stable phenotypic changes in mesangial cells because we found that mesangial cells isolated from 28-month-old mice expressed higher levels of RANTES and VCAM-1 than cells from 5-month-old mice. The elevated serum tumor necrosis factor (TNF)-alpha levels present in aged mice may contribute to increased RANTES and VCAM-1 expression in mesangial cells. Furthermore, cells from 28-month-old mice were more sensitive to TNF-alpha-induced RANTES and VCAM-1 up-regulation. The effect of TNF-alpha on RANTES expression was mediated by TNF receptor 1. Interestingly, mesangial cells isolated from 28-month-old mice had increased nuclear factor-kappaB transcriptional activity. Inhibition of nuclear factor-kappaB activity decreased baseline as well as TNF-alpha-induced RANTES and VCAM-1 expression in mesangial cells isolated from 28-month-old mice. Thus, phenotypic changes in mesangial cells may predispose them to inflammatory stimuli, such as TNF-alpha, which would contribute to glomerular macrophage infiltration and inflammatory lesions in aging.

Aging↗

PubMed2004

Adaptive and robust controller design for uncertain nonlinear systems via fuzzy modeling approach.

The issue for designing robust adaptive stabilizing controllers for nonlinear systems in Takagi-Sugeno fuzzy model with both parameter uncertainties and external disturbances is studied in this paper. It is assumed that the parameter uncertainties are norm-bounded and may be of some structure properties and that the external disturbances satisfy matching conditions and, besides, are also norm-bounded, but the bounds of the external disturbances are not necessarily known. Two adaptive controllers are developed based on linear matrix inequality technique and it is shown that the controllers can guarantee the state variables of the closed loop system to converge, globally, uniformly and exponentially, to a ball in the state space with any pre-specified convergence rate. Furthermore, the radius of the ball can also be designed to be as small as desired by tuning the controller parameters. The effectiveness of our approach is verified by its application in the control of a continuous stirred tank reactor.

Journal Article↗

PubMed2004

Development of albuminuria and glomerular lesions in normoglycemic B6 recipients of db/db mice bone marrow: the role of mesangial cell progenitors.

The pathologic hallmarks of diabetic nephropathy are excess mesangial extracellular matrix (ECM) and mesangial cell proliferation. We previously showed that mesangial cell phenotypic changes play an important role in the pathogenesis of diabetic nephropathy. We concluded that phenotypic changes were present in bone marrow (BM)-derived mesangial cell progenitors, as transplantation of BM from db/db mice, a model of type 2 diabetic nephropathy, transferred the db genotype and a nephropathy phenotype to naive B6 mice recipients. The recipients did not develop diabetes; however, they did develop albuminuria and glomerular lesions mirroring those in the donors (i.e., glomerular hypertrophy, increased ECM, and increased cell number with cell proliferation). We found that matrix metalloproteinase 2 (MMP-2) facilitated invasion of the mesangial cells into ECM and proliferation in vitro. Thus, increased MMP-2 activity in db/db mesangial cell progenitors may partially explain increased mesangial cell repopulation and proliferation in B6 recipients of db/db BM. In summary, BM-derived mesangial cell progenitors may play a crucial role in the development and progression of ECM accumulation and mesangial cell proliferation in this model of diabetic nephropathy in type 2 diabetes.

Albuminuria↗

PubMed2003

The molecular basis of age-related kidney disease.

Renal disease affects 11% of people in the United States over the age of 65, not including those with diabetes or hypertension. Although glomerular disease is the most common underlying etiology of age-related renal dysfunction, the cause of glomerular disease and whether it is the only contributor to renal failure are not known. Our studies in female mice show that renal disease in the postmenopausal period is associated with progressive glomerular enlargement and scarring, as well as abnormal renal function. To study the underlying causes of aging-related glomerular disease, we isolated and characterized glomerular smooth muscle (mesangial) cells from female mice of various ages. We found that the cells from older mice exhibit a variety of phenotypic changes, including increased concentrations of p27, a protein that serves to inhibit progression from the G1 to the S phase of the cell cycle. Because the bone marrow (BM) contains mesangial cell progenitors that can transfer the donor glomerular phenotype (normal or diseased) to recipients, we exchanged BM between postmenopausal and premenopausal mice and found that aging-related glomerular enlargement and scarring are transferred to young recipient glomeruli. In addition, BM from normal, young donors led to the regression of aging-related glomerular disease in postmenopausal recipients; namely, both glomerular enlargement and scarring were reduced. Thus, aging-related glomerular disease is an entity distinct from all other causes of renal disease, is characterized by phenotypic changes in mesangial cell progenitors, and is reversible when the phenotype of the progenitors is returned to normal.

Aged↗