- Parathyroid Disorders and Treatments
- Chronic Kidney Disease and Diabetes
- Autophagy in Disease and Therapy
- TGF-β signaling in diseases
- Renal and related cancers
- Pancreatic function and diabetes
- Genetic and Kidney Cyst Diseases
- Cancer, Hypoxia, and Metabolism
- Acute Kidney Injury Research
- Genetic Syndromes and Imprinting
- MicroRNA in disease regulation
- Advanced Glycation End Products research
- Bee Products Chemical Analysis
- Dialysis and Renal Disease Management
- Fibroblast Growth Factor Research
- Magnesium in Health and Disease
- Endoplasmic Reticulum Stress and Disease
- Peroxisome Proliferator-Activated Receptors
- Biomedical Research and Pathophysiology
- Connective Tissue Growth Factor Research
- Exercise and Physiological Responses
- Biochemical Acid Research Studies
- Renal Diseases and Glomerulopathies
- Kruppel-like factors research
- Chemotherapy-induced organ toxicity mitigation
Guiyang Medical University
2016-2025
Affiliated Hospital of Guizhou Medical University
2025
The University of Texas Southwestern Medical Center
2009-2024
Florida State University
2024
Soft-tissue calcification is a prominent feature in both chronic kidney disease (CKD) and experimental Klotho deficiency, but whether deficiency responsible for the CKD unknown. Here, wild-type mice with had very low renal, plasma, urinary levels of Klotho. In humans, we observed graded reduction starting at an early stage progressing loss renal function. Despite induction CKD, transgenic that overexpressed preserved Klotho, enhanced phosphaturia, better function, much less compared CKD....
Klotho has profound effects on phosphate metabolism, but the mechanisms of how affects homeostasis is unknown. We detected in proximal tubule cell, brush border, and urinary lumen, where resides. Increasing kidney urine chronically by transgenic overexpression or acutely intravenous infusion caused hypophosphatemia, phosphaturia from decreased reabsorption, activity protein principal renal transporter NaPi-2a. The phosphaturic effect was present FGF23-null mice, indicating a direct action...
Fibroblast growth factor (FGF) 23 inhibits renal phosphate reabsorption by activating FGF receptor (FGFR) 1c in a Klotho-dependent fashion. The phosphaturic activity of FGF23 is abrogated proteolytic cleavage at the RXXR motif that lies boundary between core homology domain and 72-residue-long C-terminal tail FGF23. Here, we show soluble ectodomains FGFR1c Klotho are sufficient to form ternary complex with vitro. mediates binding de novo site generated composite FGFR1c-Klotho interface....
Cardiac dysfunction in CKD is characterized by aberrant cardiac remodeling with hypertrophy and fibrosis. a state of severe systemic Klotho deficiency, restoration attenuates vascular calcification associated CKD. We examined the role models deficiency—genetic hypomorphism, high dietary phosphate intake, aging, Klotho-deficient mice exhibited before 12 weeks age followed In wild-type mice, induction led to cardiovascular changes not observed control mice. Notably, non-CKD fed high-phosphate...
αKlotho is a multifunctional protein highly expressed in the kidney. Soluble released through cleavage of extracellular domain from membrane by secretases to function as an endocrine/paracrine substance. The role kidney circulating production and handling incompletely understood, however. Here, we found higher concentration suprarenal compared with infrarenal inferior vena cava both rats humans. In rats, serum dropped precipitously after bilateral nephrectomy or upon treatment inhibitors...
Renal tubulointerstitial fibrosis (TIF) is a major feature of diabetic nephropathy (DN). There increasing evidence demonstrating that microRNAs act as key players in the regulation autophagy and are involved DN. However, exact link among microRNAs, autophagy, TIF DN largely unknown. In this study, our results showed was observed rats together with obvious suppression. Moreover, microRNA-22 (miR-22) upregulated associated reduced expression its target gene phosphatase tensin homolog (PTEN)...
Ectopic lipid accumulation in renal tubules is closely related to the pathogenesis of diabetic kidney disease (DKD), and mitochondrial dysfunction thought play a key role accumulation. Therefore, maintaining homeostasis holds considerable promise as therapeutic strategy for treatment DKD. Here, we report that Meteorin-like (Metrnl) gene product mediates has potential We confirmed reduced expression Metrnl tubules, which was inversely correlated with DKD pathological changes human patients...
Transforming growth factor-β1 (TGF-β1) signaling has been shown to play a critical role in the development of diabetic nephropathy (DN). The nuclear transcription co-repressor Ski-related novel protein N (SnoN) is an important negative regulator TGF-β1/Smad signal transduction, and subsequent biological responses including tubule epithelial-mesenchymal transition (EMT), extracellular matrix accumulation tubulointerstitial fibrosis. Oxymatrine (OM) alkaloid extracted from Chinese herb Sophora...
Autosis is a distinct form of cell death that requires both autophagy genes and the Na+,K+-ATPase pump. However, relationship between machinery unknown. We explored hypothesis interacts with protein Beclin 1 during stress autosis-inducing conditions. Starvation increased 1/Na+,K+-ATPase interaction in cultured cells, this was blocked by cardiac glycosides, inhibitors Na+,K+-ATPase. Increases were also observed tissues from starved mice, livers patients anorexia nervosa, brains neonatal rats...
Abstract Tubulointerstitial fibrosis (TIF) is involved in the development of diabetic kidney disease (DKD). Transforming growth factor β1 (TGF-β1) extensive renal tissue by facilitating partial epithelial-mesenchymal transition (EMT), increasing synthesis extracellular matrix (ECM), inhibiting degradation, inducing apoptosis parenchyma cells, and activating interstitial fibroblasts inflammatory cells. Recent studies indicated that bone morphogenetic protein-7 (BMP-7) upregulated expression...
Impaired wound healing and ulcer complications are major causes of morbidity in patients with diabetes. is associated increased inflammation poor angiogenesis diabetes patients. Here, we demonstrate that topical administration a secreted recombinant protein (Meteorin-like [Metrnl]) accelerates epithelialization mice. We observed significant increase Metrnl expression during physiological healing; however, its remained low diabetic healing. Functionally, the significantly accelerated closure...
Cellular senescence is an irreversible cell growth arrest and associated with aging age-related diseases. High plasma phosphate (Pi) deficiency of Klotho contribute to kidney fibrosis, a pathological feature in the chronic disease. This study examined interactive role Pi fibrosis. Homozygous hypomorphic mice had high Pi, undetectable kidney, massive collagen accumulation tubules, fibrin deposits peritubular capillaries. To examine effect on senescence, (2%) diet was given wild-type mice....
Diabetic kidney disease is a major cause of chronic condition and the most common complication diabetes. The cellular senescence participates in process diabetic disease, but specific mechanism not yet clear. Cell cycle-related protein E2F transcription factor 1 (E2F1) member family, it plays key role damage under HG conditions. In this study, we explored whether metformin improves high-glucose-induced fibrosis renal tubular epithelial cells through cell E2F1. vivo experiments, recombinant...
Cardiovascular disease (CVD) is the major cause of death in chronic kidney (CKD) and associated with high circulating fibroblast growth factor (FGF)23 levels. It unresolved whether FGF23 a mere biomarker or pathogenically contributes to cardiomyopathy. also unknown C-terminal peptide (cFGF23), natural antagonist proteolyzed from intact (iFGF23), retards CKD progression improves We addressed these questions three murine models endogenous First, we examined wild-type (WT) mice induced by...
Obesity is one of the most common metabolic diseases around world, which distinguished by abnormal buildup triglycerides within adipose cells. Recent research has revealed that autophagy regulates lipid mobilization to maintain energy balance. TIGAR (Trp53 induced glycolysis regulatory phosphatase) been identified as a inhibitor, whether it plays role in metabolism lipids unknown. Here, we found transgenic (TIGAR
C-reactive protein (CRP), was recently reported to be closely associated with poor renal function in patients acute kidney injury (AKI), but whether CRP is pathogenic or a mere biomarker AKI remains largely unclear. Impaired autophagy known exacerbate ischemia-reperfusion (IRI). We examined the role of reduction autophagy. mated transgenic rabbit over-expressing mice (Tg-CRP) two reporter mouse lines, Tg-GFP-LC3 (LC3) and Tg-RFP-GFP-LC3 (RG-LC3) respectively generate Tg-CRP-GFP-LC3 (PLC3)...