Immune-endocrine crossroads: the impact of nuclear receptors in Tuberculosis and Chagas disease DOI Creative Commons
Ana Rosa Pérez, Óscar Bottasso, Natalia Santucci

et al.

Frontiers in Endocrinology, Journal Year: 2025, Volume and Issue: 16

Published: Feb. 7, 2025

Nuclear Receptors (NRs) comprise a superfamily of proteins with essential roles in cell signaling, survival, proliferation, and metabolism. They act as transcription factors are subclassified into families based on their ligands, DNA-binding sequences, tissue specificity, functions. Evidence indicates that infectious diseases, cancer, autoimmunity, NRs modulate immune endocrine responses, altering the transcriptional profile cells organs influencing disease progression. Chronic characterized by pathogen persistence, particularly notable for an exaggerated inflammatory process. Unlike acute inflammation, which helps host respond to pathogens, chronic inflammation leads metabolic disorders dysregulated neuro-immuno-endocrine response. Over time, disturbances cytokine, hormone, other compound production foster unbalanced, detrimental defensive This complexity underscores significant role ligand-dependent NRs. Tuberculosis Chagas Disease two critical infections. The causative agents, Mycobacterium tuberculosis Trypanosoma cruzi , have developed evasion strategies establish Their clinical manifestations associated disrupted immuno-endocrine pointing potential involvement review explores current understanding regulating immune-endocrine interactions within context Disease. These diseases remain global health concerns, developing countries, highlighting importance molecular mechanisms underlying host-pathogen mediated

Language: Английский

Cultivated Enterococcus faecium B6 from children with obesity promotes nonalcoholic fatty liver disease by the bioactive metabolite tyramine DOI Creative Commons
Jia Wang, Jiayou Luo, Fei Yang

et al.

Gut Microbes, Journal Year: 2024, Volume and Issue: 16(1)

Published: May 13, 2024

Gut microbiota plays an essential role in nonalcoholic fatty liver disease (NAFLD). However, the contribution of individual bacterial strains and their metabolites to childhood NAFLD pathogenesis remains poorly understood. Herein, critical bacteria children with obesity accompanied by were identified microbiome analysis. Bacteria abundant group systematically assessed for lipogenic effects. The underlying mechanisms microbial-derived investigated using multi-omics LC-MS/MS roles crucial metabolite validated vitro vivo as well additional cohort. results showed that Enterococcus spp. was enriched NAFLD. patient-derived faecium B6 (E. B6) significantly contributed symptoms mice. E. produced a bioactive metabolite, tyramine, which probably activated PPAR-γ, leading lipid accumulation, inflammation, fibrosis liver. Moreover, these findings successfully This pioneering study elucidated important functions cultivated its (tyramine) exacerbating These advance comprehensive understanding provide new insights development microbe/metabolite-based therapeutic strategies.

Language: Английский

Citations

6
Selenomethionine protects the liver from dietary deoxynivalenol exposure via Nrf2/PPARγ-GPX4-ferroptosis pathway in mice DOI

Shijie Fan,

Luxi Lin,

Pingyang Li

et al.

Toxicology, Journal Year: 2023, Volume and Issue: 501, P. 153689 - 153689

Published: Nov. 30, 2023

Language: Английский

Citations

16
The Role of Nuclear Receptors in the Pathogenesis and Treatment of Non-alcoholic Fatty Liver Disease DOI Creative Commons
Zhenhua Yang, Awang Danzeng,

Qiumeng Liu

et al.

International Journal of Biological Sciences, Journal Year: 2023, Volume and Issue: 20(1), P. 113 - 126

Published: Nov. 15, 2023

Non-alcoholic fatty liver disease (NAFLD) is a global health burden closely linked to insulin resistance, obesity, and type 2 diabetes. The complex pathophysiology of NAFLD involves multiple cellular pathways molecular factors. Nuclear receptors (NRs) have emerged as crucial regulators lipid metabolism inflammation in NAFLD, offering potential therapeutic targets for NAFLD. Targeting PPARs FXRs has shown promise ameliorating symptoms halting progression. However, further investigation needed address side effects personalize therapy approaches. This review summarizes the current understanding involvement NRs pathogenesis explores their potential. We discuss role several modulating homeostasis liver, including peroxisome proliferator-activated (PPARs), X (LXRs), farnesoid (FXRs), REV-ERB, hepatocyte nuclear factor 4α (HNF4α), constitutive androstane receptor (CAR) pregnane (PXR).The expanding knowledge offers new avenues targeted therapies, necessitating exploration novel treatment strategies optimization existing approaches combat this increasingly prevalent disease.

Language: Английский

Citations

15
Harnessing peroxisome proliferator-activated receptor γ agonists to induce Heme Oxygenase-1: a promising approach for pulmonary inflammatory disorders DOI Creative Commons
I‐Ta Lee, Chien-Chung Yang, Chuen‐Mao Yang

et al.

Cell Communication and Signaling, Journal Year: 2024, Volume and Issue: 22(1)

Published: Feb. 15, 2024

Abstract The activation of peroxisome proliferator-activated receptor (PPAR)-γ has been extensively shown to attenuate inflammatory responses in conditions such as asthma, acute lung injury, and respiratory distress syndrome, demonstrated animal studies. However, the precise molecular mechanisms underlying these inhibitory effects remain largely unknown. upregulation heme oxygenase-1 (HO-1) confer protective effects, including antioxidant, antiapoptotic, immunomodulatory vitro vivo. PPARγ is highly expressed not only adipose tissues but also various other tissues, pulmonary system. Thiazolidinediones (TZDs) are selective agonists for used antihyperglycemic medications. These observations suggest that could modulate metabolism inflammation. Several studies have indicated may serve potential therapeutic candidates inflammation-related diseases by upregulating HO-1, which turn modulates responses. In system, exposure external insults triggers expression molecules, cytokines, chemokines, adhesion matrix metalloproteinases, reactive oxygen species, leading development diseases. Previous HO-1 protects cells from insults, indicating induction exert inhibiting signaling pathways attenuating TZD-induced well understood. This review aimed elucidate through induce explore how they protect against oxidative

Language: Английский

Citations

5
Stachyose ameliorates obesity-related metabolic syndrome via improving intestinal barrier function and remodeling gut microbiota DOI Creative Commons
Ningning He, Haoyu Wang, Shengnan Yu

et al.

Journal of Functional Foods, Journal Year: 2024, Volume and Issue: 115, P. 106106 - 106106

Published: March 7, 2024

In this study, oral supplementation of stachyose significantly improved HFD-induced MetS symptom, including overweight, hyperlipidemia, hepatic steatosis and system-wide inflammation. The subsequent analysis revealed that supplement enhanced the integrity intestinal epithelial barrier effectively reversed gut microbiota dysbiosis, as evidenced by improvements in microbial gene richness, composition, functional characteristics. abundance butyrate-producing strains, such Bacteroides faecis, Butyomonas faecalis, Parabacteroides distasonis Phocaeicola coprophilus is increased, concurrently with activation PPAR-γ signaling pathway. findings our study suggest exhibits potential a prebiotic agent for prevention dysbiosis disruption obese. results demonstrates mitigating preserving individuals MetS.

Language: Английский

Citations

5
Supplementation of Micro- and Macronutrients—A Role of Nutritional Status in Non-Alcoholic Fatty Liver Disease DOI Open Access
Magdalena Tyczyńska, Gabriela Hunek,

Martyna Szczasny

et al.

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(9), P. 4916 - 4916

Published: April 30, 2024

Non-alcoholic fatty liver disease (NAFLD) is a condition in which the pathological cumulation of fat with coexisting inflammation and damage hepatic cells leads to progressive dysfunctions liver. Except for commonly well-known major causes NAFLD such as obesity, dyslipidemia, insulin resistance, or diabetes, an unbalanced diet imbalanced nutritional status should also be taken into consideration. In this narrative review, we summarized current knowledge regarding micro- macronutrient patients suffering from considering various diets supplementation chosen supplements. We aimed summarize indicating impairments may associated onset progression at same time evaluating potential therapy targets that could facilitate healing process. above-mentioned objectives, one most important aspects review was highlight possible strategies taking care account challenges opportunities micronutrient patients. The research indicates vitamins (e.g., vitamin A, B complex, C, D) well elements zinc alleviate symptoms NAFLD. However, there still lack sufficient data healthy ranges dosages; thus, further high importance matter.

Language: Английский

Citations

4
TRIM45 facilitates NASH-progressed HCC by promoting fatty acid synthesis via catalyzing FABP5 ubiquitylation DOI
Xiaomian Li, Wenzhi He, Xi Chen

et al.

Oncogene, Journal Year: 2024, Volume and Issue: 43(27), P. 2063 - 2077

Published: May 16, 2024

Language: Английский

Citations

4
Investigation of in vitro protective effects of Mucor racemosus-fermented pine pollen on alcoholic fatty liver and its bioactive components DOI
Ziyi Zhang, Yang Chen, Qiquan Qiao

et al.

Food Bioscience, Journal Year: 2025, Volume and Issue: unknown, P. 105840 - 105840

Published: Jan. 1, 2025

Language: Английский

Citations

0
Multi‐miRNAs‐Mediated Hepatic Lepr Axis Suppression: A Pparg–Dicer1 Pathway‐Driven Mechanism in Spermatogenesis for the Intergenerational Transmission of Paternal Metabolic Syndrome DOI Creative Commons
Yi Lin, Xiuye Ni, Lin Zhu

et al.

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

Published: Jan. 10, 2025

Abstract Bisphenol A (BPA) is an “environmental obesogen” and this study aims to investigate the intergenerational impacts of BPA‐induced metabolic syndrome (MetS), specifically focusing on unraveling mechanisms. Exposure BPA induces disorders in paternal mice, which are then transmitted offspring, leading late‐onset MetS. Mechanistically, upregulates Srebf1, turn promotes Pparg‐dependent transcription Dicer1 spermatocytes, increasing levels multiple sperm microRNAs (miRNAs). Several these miRNAs highly expressed a synchronized manner liver offspring. miR149‐5p, miR150‐5p, miR700‐5p target specific region Lepr 3′UTR, termed “SMITE” (“ S everal Mi RNAs T argeting E lements”), negatively regulate Lepr. These i nherited nti‐ L epr miRNAs, also referred (IAL‐miRs), modulate hepatic steatosis, insulin signaling through regulatory Igfbp2, Egfr, Ampk. Furthermore, IAL‐miRs inhibit Ccnd1 not only via binding but Lepr–Igfbp2 axis, contribute hepatocyte senescence. pathological processes interact self‐reinforcing cycle, worsening MetS BPA‐exposed The findings reveal mechanism wherein lipid metabolism reprogramming spermatocytes‐induced perturbations triggered by BPA, leads inheritance suppression axis

Language: Английский

Citations

0
Yinchen lipid-lowering tea attenuates lipid deposition in a fatty liver model by regulating mitochondrial dysfunction through activation of AdipoR1/AMPK/SIRT1 signaling DOI Creative Commons

Xinhua Luo,

Yihang Fang,

Wei Wang

et al.

3 Biotech, Journal Year: 2025, Volume and Issue: 15(2)

Published: Jan. 13, 2025

Abstract This study investigated the ameliorative effects of Yinchen lipid-lowering tea (YCLLT) on Non-alcoholic fatty liver disease (NAFLD), specific mechanism involved was also studied. We modeled hepatocellular steatosis with HepG2 cells and intervened different concentrations YCLLT-containing serum. Lipid deposition assessed by oil red O staining AdipoR1 expression analyzed Western blot. The hepatocyte model further treated serum and/or silencing AdipoR1. observed staining. Flow cytometry used to detect apoptosis mitochondrial membrane potential. levels TNF-α, IL-6, MDA, 8-OHdG, ATP were ELISA or corresponding kits. structure transmission electron microscopy. AdipoR1/AMPK/SIRT1 signaling pathway factors blot, co-localization SIRT1 immunofluorescence. results revealed that YCLLT attenuated lipid deposition, inhibited inflammatory TNF-α reduced MDA up-regulated content potential, promoted AdipoR1, p-LKB1, p-AMPKα, SIRT1, PGC-1a in a cellular NAFLD. Further, effect NAFLD cell model. Altogether, attenuates improving function via activating AdipoR1/AMPK/ signaling.

Language: Английский

Citations

0