Cited by Correction to: Increased RTN3 phenocopies nonalcoholic fatty liver disease by inhibiting the AMPK‐IDH2 pathway

Ferroptosis: an important player in the inflammatory response in diabetic nephropathy DOI

Jialing Li, Luxin Li, Zhen Zhang

et al.

Frontiers in Immunology, Journal Year: 2023, Volume and Issue: 14

Published: Dec. 4, 2023

Diabetic nephropathy (DN) is a chronic inflammatory disease that affects millions of diabetic patients worldwide. The key to treating DN early diagnosis and prevention. Once the patient enters clinical proteinuria stage, renal damage difficult reverse. Therefore, developing treatment methods critical. pathogenesis results from various factors, among which immune response inflammation play major roles. Ferroptosis newly discovered type programmed cell death characterized by iron-dependent lipid peroxidation excessive ROS production. Recent studies have demonstrated activation closely related occurrence development ferroptosis. Moreover, hyperglycemia induces iron overload, peroxidation, oxidative stress, inflammation, fibrosis, all are pathogenesis, indicating ferroptosis plays role in DN. this review focuses on regulatory mechanisms ferroptosis, mutual processes involved inflammation. By discussing analyzing relationship between DN, we can deepen our understanding develop new therapeutics targeting or inflammation-related for with

Language: Английский

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Increased RTN3 phenocopies nonalcoholic fatty liver disease by inhibiting the AMPK–IDH2 pathway DOI

Hao Huang, Shuai Guo,

Yaqin Chen

et al.

MedComm, Journal Year: 2023, Volume and Issue: 4(2)

Published: March 14, 2023

Abstract Reticulon 3 (RTN3), an endoplasmic reticulum protein, is crucial in neurodegenerative and kidney diseases. However, the role of RTN3 liver tissues has not been described. Here, we employed public datasets, patients, several animal models to explore nonalcoholic fatty disease (NAFLD). The underlying mechanisms were studied primary hepatocytes L02 cells vitro. We found increased expression NAFLD high‐fat diet mice, oxidized low‐density lipoprotein‐treated cells. transgenic mice exhibited phenotypes lipid accumulation. Single‐cell RNA sequencing analysis indicated that might induce mitochondrial dysfunction. further showed this hepatocytes, cell line, Caenorhabditis elegans strain. Mechanistically, regulated these events through its interactions with glucose‐regulated protein 78 (GRP78), which inhibited adenosine 5 monophosphate‐activated kinase (AMPK)–isocitrate dehydrogenase 2 (IDH2) pathway. In end, knockout relieved Our study was important catabolism increase be a risk factor for steatohepatitis NAFLD.

Language: Английский

Citations

Poria cocos: traditional uses, triterpenoid components and their renoprotective pharmacology DOI

Zhi-yuan Guo,

X. Wu,

Shui-juan Zhang

et al.

Acta Pharmacologica Sinica, Journal Year: 2024, Volume and Issue: unknown

Published: Oct. 31, 2024

Language: Английский

Citations

Cell therapy in end-stage liver disease: replace and remodel DOI

Xin-Hao Hu,

Lan Chen, Hao Wu

et al.

Stem Cell Research & Therapy, Journal Year: 2023, Volume and Issue: 14(1)

Published: May 25, 2023

Abstract Liver disease is prevalent worldwide. When it reaches the end stage, mortality rises to 50% or more. Although liver transplantation has emerged as most efficient treatment for end-stage disease, its application been limited by scarcity of donor livers. The lack acceptable organs implies that patients are at high risk while waiting suitable In this scenario, cell therapy a promising approach. Most time, transplanted cells can replace host hepatocytes and remodel hepatic microenvironment. For instance, derived from livers stem colonize proliferate in liver, hepatocytes, restore function. Other cellular candidates, such macrophages mesenchymal cells, microenvironment, thereby repairing damaged liver. recent years, transitioned animal research early human studies. review, we will discuss treatment, especially focusing on various types utilized transplantation, elucidate processes involved. Furthermore, also summarize practical obstacles offer potential solutions.

Language: Английский

Citations

Accumulation of neutral lipids in dystrophic neurites surrounding amyloid plaques in Alzheimer's disease DOI

Hao Huang, Md Golam Sharoar,

Joseph Pathoulas

et al.

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Journal Year: 2024, Volume and Issue: 1870(4), P. 167086 - 167086

Published: Feb. 18, 2024

Language: Английский

Citations

Early‐life antibiotic exposure aggravates hepatic steatosis through enhanced endotoxemia and lipotoxic effects driven by gut Parabacteroides DOI

Xi Zhang,

Darren Chan,

Jie Zhu

et al.

MedComm, Journal Year: 2025, Volume and Issue: 6(3)

Published: Feb. 17, 2025

Abstract Compelling evidence supports a link between early‐life gut microbiota and the metabolic outcomes in later life. Using an antibiotic exposure model BALB/c mice, we investigated life‐course impact of prenatal and/or postnatal exposures on microbiome offspring development dysfunction‐associated steatotic liver disease (MASLD). Compared to alone, more profoundly affected succession, which led aggravated endotoxemia dysfunctions. This was primarily resulted from overblooming Parabacteroides hepatic accumulation cytotoxic lysophosphatidyl cholines (LPCs), acted conjunction with LPS derived distasonis (LPS_PA) induce cholesterol dysregulations, endoplasmic reticulum (ER) stress apoptosis. Integrated serum metabolomics, lipidomics transcriptomics revealed enhanced glycerophospholipid hydrolysis LPC production association upregulation PLA2G10, gene controlling expression group X secretory Phospholipase A2s (sPLA2‐X). Taken together, our results show microbial modulations systemic MASLD pathogenesis hepatocellular lipotoxicity pathways following exposure, hence help inform refined clinical practices avoid any prolonged maternal administration early life potential microbiota‐targeted intervention strategies.

Language: Английский

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Integrated Analysis of WES and scRNA‐Seq Data Reveals the Genetic Basis of Immune Dysregulation in Unexplained Recurrent Pregnancy Loss DOI

Zhiming Lin,

Lei Zhu,

Dong Yi

et al.

Journal of Clinical Laboratory Analysis, Journal Year: 2025, Volume and Issue: unknown

Published: March 11, 2025

ABSTRACT Objective This study aimed to identify genetic variants and their functional consequences underlying Unexplained Recurrent Pregnancy Loss (uRPL) through comprehensive genomic transcriptomic analyses. Methods We recruited 13 Chinese uRPL patients performed Whole Exome Sequencing (WES) on chorionic villi samples from miscarriage tissues. Additionally, we conducted an integrative analysis using single‐cell RNA sequencing data decidual immune cells examine expression patterns. Results WES pinpointed in the four MUC genes ( MUC4 , MUC6 MUC16 MUC17 ), six lipid metabolism ABCA4 ABCA7 ABCB5 ABCC8 ADGRV1 ANK3 two structural PIEZO1 PKD1 whose impair mucosal barriers homeostasis, thereby leading dysregulation contributing uRPL. To delve deeper into effects of these cellular patterns, undertook a dataset cases. observed significant within cells, reduced heat shock protein expression, enhanced chemokine signaling samples, indicating pro‐inflammatory state. Conclusions In summary, our reveals complex interplay between cell dysfunctions uRPL, emphasizing role identified driving states. These findings provide view molecular mechanisms opening paths for novel therapeutic interventions improved clinical management.

Language: Английский

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Deletion of Pyruvate Carboxylase in Tubular Epithelial Cell Promotes Renal Fibrosis by Regulating SQOR/cGAS/STING‐Mediated Glycolysis DOI

Hao Huang, Yuanyuan Han, Yan Zhang

et al.

Advanced Science, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 21, 2025

Abstract Renal fibrosis is a common pathway involved in the progression of various chronic kidney diseases to end‐stage renal disease. Recent studies show that mitochondrial injury tubular epithelial cells (RTECs) crucial pathological foundation for fibrosis. However, underlying regulatory mechanisms remain unclear. Pyruvate carboxylase (PC) catalytic enzyme located within mitochondria intricately linked with damage and metabolism. In present study, downregulation PC fibrotic animal human samples demonstrated. proximal tubule–specific Pcx gene knockout mice ( cKO ) has significant interstitial compared control mice, heightened expression extracellular matrix molecules. This further demonstrated stable knock‐out RTEC line. Mechanistically, deficiency reduces its interaction sulfide:quinone oxidoreductase (SQOR), increasing ubiquitination degradation SQOR. leads morphological functional disruption, increased mtDNA release, activation cGAS‐STING pathway, elevated glycolysis levels, ultimately, promotes study investigates molecular through which induces metabolic reprogramming RTECs. provides novel theoretical potential therapeutic targets pathogenesis treatment

Language: Английский

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RTN3 regulates collagen biosynthesis and profibrotic macrophage differentiation to promote pulmonary fibrosis via interacting with CRTH2 DOI

Chenyu Wang,

Yaqin Chen,

Hao Huang

et al.

Molecular Medicine, Journal Year: 2025, Volume and Issue: 31(1)

Published: Feb. 19, 2025

Language: Английский

Citations

Characterization of macrophages in ischemia–reperfusion injury-induced acute kidney injury based on single-cell RNA-Seq and bulk RNA-Seq analysis DOI

Qin Wang, Yuxing Liu, Yan Zhang

et al.

International Immunopharmacology, Journal Year: 2024, Volume and Issue: 130, P. 111754 - 111754

Published: March 1, 2024

Language: Английский

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