Yachun Han

ORCID: 0000-0002-8165-6698
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Research Areas
  • Chronic Kidney Disease and Diabetes
  • Autophagy in Disease and Therapy
  • Endoplasmic Reticulum Stress and Disease
  • Advanced Glycation End Products research
  • Mitochondrial Function and Pathology
  • Heme Oxygenase-1 and Carbon Monoxide
  • Renal Diseases and Glomerulopathies
  • Biomedical Research and Pathophysiology
  • Genetic and Kidney Cyst Diseases
  • Inflammasome and immune disorders
  • Adipose Tissue and Metabolism
  • Renal and related cancers
  • Cancer, Hypoxia, and Metabolism
  • Ferroptosis and cancer prognosis
  • Cholesterol and Lipid Metabolism
  • Pancreatic function and diabetes
  • Eicosanoids and Hypertension Pharmacology
  • Lipid metabolism and disorders
  • COVID-19 Impact on Reproduction
  • Diabetes and associated disorders
  • Adipokines, Inflammation, and Metabolic Diseases
  • Diabetes Treatment and Management
  • Vitamin D Research Studies
  • Metabolism and Genetic Disorders
  • Chemotherapy-induced organ toxicity mitigation

Second Xiangya Hospital of Central South University
2015-2025

Central South University
2016-2025

Soil and Fertilizer Institute of Hunan Province
2021-2024

Agricultural Genomics Institute at Shenzhen
2023

Chinese Academy of Agricultural Sciences
2023

Third Xiangya Hospital
2018-2022

Xiangya Hospital Central South University
2016-2022

NLRP3/IL-1β activation via thioredoxin (TRX)/thioredoxin-interacting protein (TXNIP) following mitochondria ROS (mtROS) overproduction plays a key role in inflammation. However, the involvement of this process tubular damage kidneys patients with diabetic nephropathy (DN) is unclear. Here, we demonstrated that mtROS accompanied by decreases TRX expression and TXNIP up-regulation. In addition, discovered also associated increases TGF-β DN db/db mice. We reversed these changes mice...

10.1016/j.redox.2018.02.013 article EN cc-by-nc-nd Redox Biology 2018-02-15

Abstract Renal tubulointerstitial fibrosis was a crucial pathological feature of diabetic nephropathy (DN), and renal tubular injury might associate with abnormal mitophagy. In this study, we investigated the effects molecular mechanisms AMPK agonist metformin on mitophagy cellular in cell under condition. The high fat diet (HFD) streptozotocin (STZ)-induced type 2 mice model HK-2 cells were used study. Metformin administered drinking water (200 mg/kg/d) for 24 weeks. lesions, oxidative...

10.1038/s41419-021-04184-8 article EN cc-by Cell Death and Disease 2021-10-09

Abstract Objectives In diabetic nephropathy (DN), hypoxia‐inducible factor‐1α (HIF‐1α) activation in tubular cells plays an important protective role against kidney injury. The effects may occur via the target genes of HIF‐1α, such as haem oxygenase‐1 (HO‐1), but exact mechanisms are incompletely understood. Materials and methods Mice with proximal tubule‐specific knockout HIF‐1α (PT‐HIF‐1α −/− mice) were generated, diabetes was induced these mice by streptozotocin (STZ) injection. addition,...

10.1111/cpr.12909 article EN cc-by Cell Proliferation 2020-09-25

Abstract Autophagy-mediated lipotoxicity plays a critical role in the progression of diabetic nephropathy (DN), but precise mechanism is not fully understood. Whether lipophagy, selective type autophagy participates renal ectopic lipid deposition (ELD) and kidney DN unknown. Here, decreased increased ELD lipotoxcity were observed tubular cells patients with DN, which accompanied reduced expression AdipoR1 p-AMPK. Similar results found db/db mice, these changes reversed by AdipoRon, an...

10.1038/s41419-021-04326-y article EN cc-by Cell Death and Disease 2021-10-30

Mitochondria-associated endoplasmic reticulum membrane (MAM) may have a role in tubular injury diabetic nephropathy (DN), but the precise mechanism remains unclear. Here, we demonstrate that expression of phosphofurin acidic cluster sorting protein 2 (PACS-2), critical regulator MAM formation, is significantly decreased renal tubules patients with DN, and PACS-2 positively correlated function negatively degrees tubulointerstitial lesions. Conditional deletion Pacs-2 proximal (PTs) aggravates...

10.2337/db21-0983 article EN Diabetes 2022-02-08

Alpha-kinase 1 (ALPK1) is a master regulator in inflammation and has been proved to promote renal fibrosis by promoting the production of IL-1β diabetic nephropathy (DN) mice. Pyroptosis involved high glucose (HG)-induced tubular cells injury, characterized activation Gasdermin D (GSDMD) release IL-18, resulting inflammatory injury DN. It reasonable assume that ALPK1 pyroptosis-related However, mechanism remains poorly defined.Immunohistochemistry (IHC) staining was performed detect...

10.1186/s40659-023-00416-7 article EN cc-by Biological Research 2023-02-02

Diabetic nephropathy (DN) is a serious complication of diabetes mellitus and an important cause end-stage renal disease (ESRD). However, there still lack effective prevention treatment strategies in clinical practice. As metabolic disease, DN accompanied by ectopic lipid deposition, the deposited lipids further aggravate kidney injury. molecular mechanism deposition currently unknown. In this study, we observed changes droplet (LD)–mitochondria connections for first time. Destruction...

10.1021/acs.jafc.4c06122 article EN Journal of Agricultural and Food Chemistry 2025-01-07

BackgroundThe mitochondrial associated endoplasmic reticulum (ER) membrane (MAM) provides a platform for communication between the mitochondria and ER, it plays vital role in many biological functions. Disulphide-bond A oxidoreductase-like protein (DsbA-L), expressed MAM, serves as an antioxidant reduces ER stress. However, of DsbA-L MAM kidney pathobiology remains unclear.MethodsMolecular biology techniques, transmission electron microscopy (TEM), situ proximity ligation assays (PLAs),...

10.1016/j.ebiom.2019.04.044 article EN cc-by-nc-nd EBioMedicine 2019-05-01

This study aimed to assess the effect and mechanism of SS31 on cisplatin-induced acute kidney injury (CP-AKI) both in vivo vitro. Male mices HK-2 cells were treated using cisplatin establish models CP-AKI. 32 C57BL/6 randomly divided into four groups (control group, CP + normal saline SS-31 group). Cisplatin was intraperitoneally injected once mice (25 mg/kg). administrated for 10 days at dosages mg/kg per day. Kidney histological changes level reactive oxygen species(ROS) detected. In vitro...

10.1016/j.biopha.2020.110521 article EN Biomedicine & Pharmacotherapy 2020-07-24

Cisplatin is one of the major causes acute kidney injury (AKI) in clinical practice, and ferroptosis an essential form cell death cisplatin-induced AKI (CP-AKI). WW domain binding protein-2 (WBP2), a molecular chaperon, involved progression various malignancies, but its role renal injuries has not been investigated. Our present study employed bioinformatics analysis to identify WBP2 as potential modulator ferroptosis. Preliminary laboratory investigations showed that WBP2, highly expressed...

10.1016/j.redox.2023.102826 article EN cc-by-nc-nd Redox Biology 2023-07-26

Probucol is an anti-hyperlipidemic agent and a potent antioxidant drug that can delay progression of diabetic nephropathy (DN) reverses renal oxidative stress in animal models; however, the mechanisms underlying these effects remain unclear. p66Shc newly recognized mediator mitochondrial ROS production cells under high-glucose (HG) ambience. We previously showed serve as biomarker for injury DN patients up-regulation correlated with damage vivo vitro. Here, we determined whether probucol...

10.1016/j.redox.2017.07.002 article EN cc-by-nc-nd Redox Biology 2017-07-04

Renal tubular injury is an early characteristic of diabetic nephropathy (DN) that related to mitochondrial dysfunction. In this study, we explore the effects and mechanisms mitochondria-targeted peptide SS31 on renal tubulointerstitial in DN. 40 C57BL/6 mice were randomly divided into control group, STZ STZ+SS31 STZ+normal saline group. was intraperitoneally injected every other day for 24 weeks. lesions expression Drp1, Mfn1, Bcl-2, Bax, Caspase1, IL-1β, FN detected. vitro studies, HK-2...

10.1155/2019/2346580 article EN Oxidative Medicine and Cellular Longevity 2019-06-02

Abstract Cisplatin (Cis) can cause chronic kidney disease (CKD) and promote renal fibrosis, but the underlying mechanism is not fully understood. Hypoxia inducible factor-1α (HIF-1α) fibrosis in some diseases, its role Cis-induced CKD still unknown. Notch-1 a recognized molecule that promotes under pathological circumstances, evidence shows HIF-1α are closely related to each other. In present study, mice with gene knockout proximal tubular cells (PTCs) (PT-HIF-1α-KO) were generated treated...

10.1042/cs20210061 article EN cc-by Clinical Science 2021-05-01

Lipid metabolism imbalance is involved in the mechanism of renal tubular injury diabetic kidney disease (DKD). Fatty acid binding protein 4 (FABP4) has been reported to participate cellular lipid toxicity. However, expression FABP4 tissues DKD and its correlation with clinical/ pathological parameters prognosis have not studied.

10.2174/0109298673268265231228125431 article EN Current Medicinal Chemistry 2024-02-01

Abstract Increased p66Shc expression has been associated with diabetic nephropathy (DN). However, whether can serve as a potential biomarker for tubular oxidative injury in DN is unknown. We measured the of peripheral blood monocytes (PBMs) and renal biopsy tissues from patients then analysed relationship between clinical characteristics DN. Patients were divided into 4 groups (class IIa, class IIb, III control group). qPCR, Western blotting immunohistochemistry performed. The results showed...

10.1038/srep29302 article EN cc-by Scientific Reports 2016-07-05
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