A5102792130- Renal Diseases and Glomerulopathies
- Autophagy in Disease and Therapy
- Chronic Kidney Disease and Diabetes
- Acute Kidney Injury Research
- Endometriosis Research and Treatment
- Genetic and Kidney Cyst Diseases
- Tryptophan and brain disorders
- Adenosine and Purinergic Signaling
- Renal and related cancers
- Lysosomal Storage Disorders Research
- Kruppel-like factors research
- Advanced Glycation End Products research
- Stress Responses and Cortisol
- Trace Elements in Health
- Dermatology and Skin Diseases
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Organ Transplantation Techniques and Outcomes
- Amyloidosis: Diagnosis, Treatment, Outcomes
- Microplastics and Plastic Pollution
- Extracellular vesicles in disease
- Signaling Pathways in Disease
- Sesame and Sesamin Research
- Muscle metabolism and nutrition
- Vasculitis and related conditions
- Genetic Syndromes and Imprinting
Zhongkai University of Agriculture and Engineering
2025
Guangdong Academy of Medical Sciences
2016-2024
Southern Medical University
2017-2024
Guangdong Provincial People's Hospital
2019-2024
Shandong University
2024
Guangdong General Hospital
2016-2018
Nanfang Hospital
2017
Insufficient autophagy in podocytes is related to podocyte injury diabetic nephropathy (DN). Advanced glycation end-products (AGEs) are major factors of DN. However, the role and mechanism AGEs autophagic dysfunction remain unknown. We investigated flux AGE-stimulated cultured using multiple assays: western blotting, reverse transcription-quantitative PCR, immunofluorescence staining, electron microscopy. also utilized chloroquine a fluorescent probe monitor formation turnover...
Abstract Podocyte apoptosis is a major mechanism that leads to proteinuria in many chronic kidney diseases. However, the concert mechanisms cause podocyte these diseases are not fully understood. The Rho family of small GTPases has been shown be required maintaining structure and function. Recent studies have indicated podocyte-specific deletion Cdc42 vivo , but RhoA or Rac1, congenital nephrotic syndrome glomerulosclerosis. underlying cellular events controlled by remain unclear. Here, we...
ABSTRACT Skeletal muscle mass is significantly negatively regulated by glucocorticoids. Following glucocorticoid administration, the balance between protein synthesis and breakdown in skeletal disrupted, shifting towards a predominance of catabolic metabolism. Short‐chain fatty acids like sodium butyrate have been found to regulate inflammatory reactions successively activate signaling pathways. The preventive benefits against dexamethasone‐induced atrophy myotube models were examined this...
Acute kidney injury (AKI) with maladaptive tubular repair leads to renal fibrosis and progresses chronic disease (CKD). At present, there is no curative drug interrupt AKI-to-CKD progression. The nuclear factor of the activated T cell (NFAT) family was initially identified as a transcription expressed in most immune cells involved cytokine genes other critical for response. NFAT2 also epithelial (RTECs) podocytes plays an important regulatory role kidney. In this study, we investigated...
This study aimed to investigate the protective effect of necroptosis inhibitor necrosulfonamide (NSA) on intestinal epithelial cells using a novel in vitro model that mimics inflammatory bowel disease (IBD).2,4,6-trinitrobenzenesulfonic acid (TNBS) was perfused into rectum BALB/c mice established colitis model. Pathologic injury and cell death were evaluated. A Caco-2 TNF-α Z-VAD-fmk, treated with or without NSA. Morphologic changes, manner levels phosphorylation receptor-interacting protein...
Renal tubular epithelial cell apoptosis is an important pathological mechanism of septic acute kidney injury (AKI). Endotoxin, also known as lipopolysaccharide (LPS), has a key role in AKI and can directly induce apoptosis. The upregulation receptor‑interacting protein kinase 3 (RIPK3) cells been reported AKI, with RIPK3 mediating several types. In the present study, effect on endotoxin‑induced was investigated mouse vitro vivo. It found that expression markedly increased AKI....
Ischemia-reperfusion (I/R)-induced acute kidney injury (I/R-AKI) favors mitochondrial permeability transition pore (mPTP) opening and subsequent cell death. Cyclophilin D (CypD) is an essential component of the mPTP, recent findings have implicated p53-CypD complex in To evaluate role after I/R-AKI, we tested hypothesis that mediates renal tubular apoptosis I/R-AKI via mPTP opening. Expression p53 cleaved caspase-3 was significantly increased rats subjected to compared with normal controls...
Abstract Autophagy is an important renal-protective mechanism in septic acute kidney injury (AKI). Receptor interacting protein kinase 3 (RIP3) has been implicated the renal tubular and dysfunction during AKI. Here we investigated role of RIP3 on autophagy We showed activation RIP3, accompanied by accumulation autophagosome marker LC3II autophagic substrate p62, kidneys lipopolysaccharide (LPS)-induced AKI mice LPS-treated cultured proximal epithelial cells (PTECs). The lysosome inhibitor...
Diabetic kidney disease (DKD) is a serious and common complication of diabetes. Extracellular vesicles (EVs) have emerged as crucial vectors in cell-to-cell communication during the development DKD. EVs may mediate intercellular between podocytes proximal tubules. In this study, were isolated from podocyte culture supernatants under high glucose (HG), normal (NG), iso-osmolality conditions, then co-cultured with tubular epithelial cells (PTECs). MicroRNAs (miRNA) sequencing was conducted to...
Abstract Podocyte injury and loss contribute to proteinuria, glomerulosclerosis eventually kidney failure. Recent studies have demonstrated that the of Kruppel-like factor 15 (KLF15) in podocytes increases susceptibility injury; however, mechanism underlying protective effects on podocyte remains incompletely understood. Herein, we showed KLF15 ameliorates through suppressing NFAT signaling salutary synthetic glucocorticoid dexamethasone were partially mediated by KLF15–NFATc1 axis. We found...
High-level autophagy has an important role in maintaining the stable state of podocytes. The present study explored influence lipopolysaccharide (LPS) on autophagic activity podocytes and demonstrated its mechanistic involvement LPS-induced injury. Conditionally immortalized were cultured vitro treated with chloroquine (CQ), LPS, LPS+rapamycin or LPS+3‑methyladenine (3‑MA). vesicles endoplasmic reticulum observed using transmission electron microscopy. tandem mRFP‑GFP‑LC3 adenovirus was used...
// Yuanhan Chen 1 , Zhen Xie 2 Chenggen Xiao 1, 3 Min Zhang 4 Zhilian Li Jianteng Yusheng 5 Xingchen Zhao 6 Pengfei Zeng Liyi Mo 7 Xinling Liang Wei Shi Division of Nephrology, Guangdong General Hospital, Academy Medical Sciences, Guangzhou, China Department Dermatology, Sichuan Sciences & Provincial People's Chengdu, Xiangya Central South University, Hunan, Gastroenterology, The Sixth Affiliated Sun Yat-Sen Second Internal Medicine, Wuhua Guangdong, Southern Dongguan Province,...
Previous studies have indicated that glomerular podocyte injury serves a crucial role in proteinuria during the process of chronic kidney disease. The slit diaphragm podocytes forms final barrier to proteinuria. Dendrin, constituent protein complex, has been observed relocate from nuclei injured and promote apoptosis. However, exact mechanism for nuclear relocation dendrin remains unclear. expression WWC1 induced by lipopolysaccharides (LPS) or adriamycin (ADR) was detected reverse...
Nicotinamide adenine dinucleotide (NAD) is an essential coenzyme in the kidney. The first step de novo NAD synthesis regulated by indoleamine 2,3-dioxygenase (IDO), a tryptophan-catabolizing enzyme. Here, we investigated synthetic flux and levels podocytes under diabetic conditions. We also studied effects of IDO overexpression on high glucose (HG)-induced podocyte injury. synthetases novo, Preiss-Handler salvage pathways were analyzed using vivo single-nucleus RNA sequencing datasets...
Autophagy is important for maintaining normal physiological functions and podocyte cell homeostasis. Amino acid signaling an upstream pathway autophagy regulation. However, the function associated mechanism of amino in unclear. The present study used culture medium deprivation to podocytes vitro. Multiple methods were utilized detect autophagic activity including western blot analysis measure levels microtubule‑associated protein 1 light chain 3 (LC3) II beclin1, reverse...
The tryptophan‐depleting enzyme indoleamine‐2,3‐dioxygenase (IDO) is critical for the regulation of immunotolerance and plays an important role in immune‐associated skin diseases. To analyse level IDO condyloma acuminata (CA) its this condition. expression was assessed peripheral blood healthy controls patients with CA. assess immunity, ability isolated epidermal cells to metabolize tryptophan influence on polyclonal T‐cell mitogen (PHA)‐stimulated proliferation were explored. median...
Background Diabetic kidney diseases (DKD) were the leading cause of End-stage renal worldwide. Albuminuria was a target for treatment in DKD and decreasing albuminuria particularly important improving its prognosis. However, there is still lack specific DKD.Methods We conducted prospective, crossover, open-label study to investigate effect amiloride patients with DKD. Safety efficacy assessed by monitoring urine protein creatinine ratio(uPCR), urinary albumin ratio (uACR), blood pressure,...
Rationale: Focal segmental glomerulosclerosis (FSGS) describes a renal histologic lesion with diverse causes and pathogenicities. Monogenic abnormalities which are associated impaired function of podocyte could result in FSGS. Most genetic FSGS do not respond to immunosuppressive agents often develop end-stage kidney disease. We reported case caused by myosin1e (MYO1E) mutation, alleviated cyclosporine A (CsA) low-dose glucocorticoid. Patient concerns: The patient was 38-year-old male...
Podocyte injury is a common hallmark of chronic kidney disease (CKD). The podocin-nephrin complex localized in lipid rafts podocyte vital to reduce and proteinuria, however, the mechanism underlying its localization remains unclear. This study uncovers an important role Flot2 stabilizing rafts. We first confirmed that was expressed demenstrated podocyte-specific deletion worsen albuminuria, glomerular pathology LPS/ADR-induced nephropathy mouse models. Meanwhile, injury, albuminuria...