A5050155862- Acute Kidney Injury Research
- Chemotherapy-induced organ toxicity mitigation
- Autophagy in Disease and Therapy
- Cancer, Hypoxia, and Metabolism
- Chronic Kidney Disease and Diabetes
- Hormonal Regulation and Hypertension
- Cell death mechanisms and regulation
- Cancer, Lipids, and Metabolism
- Renal and related cancers
- MicroRNA in disease regulation
- Epigenetics and DNA Methylation
- Dialysis and Renal Disease Management
- Mitochondrial Function and Pathology
- Heme Oxygenase-1 and Carbon Monoxide
- Biomedical Research and Pathophysiology
- Genetic and Kidney Cyst Diseases
- Advanced Glycation End Products research
- Renal Diseases and Glomerulopathies
- Cancer-related Molecular Pathways
- Endoplasmic Reticulum Stress and Disease
- Histone Deacetylase Inhibitors Research
- Organ Transplantation Techniques and Outcomes
- Cardiac Ischemia and Reperfusion
- RNA Interference and Gene Delivery
- Acute Lymphoblastic Leukemia research
Charlie Norwood VA Medical Center
2016-2025
Augusta University
2016-2025
Second Xiangya Hospital of Central South University
2016-2025
Central South University
2016-2025
First Affiliated Hospital of Kunming Medical University
2025
Kunming Medical University
2025
Affiliated Hospital of North Sichuan Medical College
2025
North Sichuan Medical University
2025
Augusta University Health
2011-2024
Xinjiang Medical University
2024
The mechanism of mitochondrial damage, a key contributor to renal tubular cell death during acute kidney injury, remains largely unknown. Here, we have demonstrated striking morphological change mitochondria in experimental models ischemia/reperfusion and cisplatin-induced nephrotoxicity. This contributed outer membrane permeabilization, release apoptogenic factors, consequent apoptosis. Following either ATP depletion or cisplatin treatment rat cells, fragmentation was observed prior...
Mitochondria play a crucial role in tubular injury diabetic kidney disease (DKD). MitoQ is mitochondria-targeted antioxidant that exerts protective effects mice, but the mechanism underlying these not clear. We demonstrated mitochondrial abnormalities, such as defective mitophagy, reactive oxygen species (ROS) overexpression and fragmentation, occurred cells of db/db accompanied by reduced PINK Parkin expression increased apoptosis. These changes were partially reversed following an...
Mitochondrial injury, characterized by outer membrane permeabilization and consequent release of apoptogenic factors, is a key to apoptosis mammalian cells. Bax Bak, two multidomain Bcl-2 family proteins, provide requisite gateway mitochondrial injury. However it unclear how Bak cooperate provoke injury whether their roles are redundant. Here, we have identified unique role in fragmentation, seemingly morphological event that contributes during apoptosis. We show fragmentation attenuated...
The usefulness and efficacy of cisplatin, a chemotherapeutic drug, are limited by its toxicity to normal tissues organs, including the kidneys. uptake cisplatin in renal tubular cells is high, leading accumulation cell injury death, culminating acute failure. While extensive investigations have been focused on signaling pathways nephrotoxicity, much less known about mechanism tissues. In this regard, evidence has shown for involvement organic cation transporters (OCT), specifically OCT2....
Damaged or dysfunctional mitochondria are toxic to the cell by producing reactive oxygen species and releasing death factors. Therefore, timely removal of these organelles is critical cellular homeostasis viability. Mitophagy mechanism selective degradation via autophagy. The significance mitophagy in kidney diseases, including ischemic acute injury (AKI), has yet be established, involved pathway remains poorly understood. Here, we show that induced renal proximal tubular cells both vitro...
Renal fibrosis is the final, common pathway of end-stage renal disease. Whether and how autophagy contributes to remains unclear. Here we first detected persistent in kidney proximal tubules model unilateral ureteral obstruction (UUO) mice. UUO-associated was suppressed by pharmacological inhibitors also tubule-specific knockout autophagy-related 7 (PT-Atg7 KO). Consistently, proliferation activation fibroblasts, as indicated expression ACTA2/α-smooth muscle actin VIM (vimentin), inhibited...
Increased activation of the serine-glycine biosynthetic pathway is an integral part cancer metabolism that drives macromolecule synthesis needed for cell proliferation. Whether this under epigenetic control unknown. Here we show histone H3 lysine 9 (H3K9) methyltransferase G9A required maintaining enzyme genes in active state marked by H3K9 monomethylation and transcriptional response to serine deprivation. inactivation depletes its downstream metabolites, triggering death with autophagy...
Ischemic preconditioning (IPC) affords tissue protection in organs including kidneys; however, the underlying mechanism remains unclear. Here we demonstrate an important role of macroautophagy/autophagy (especially mitophagy) protective effect IPC kidneys. induced autophagy renal tubular cells mice and suppressed subsequent ischemia-reperfusion injury (IRI). The was abolished by pharmacological inhibitors ablation Atg7 from kidney proximal tubules. Pretreatment with BECN1/Beclin1 peptide...