Iron-Mediated Regulation in Adipose Tissue: A Comprehensive Review of Metabolism and Physiological Effects DOI
Xinyu Yang, Xianghong Wang, Zhe Yang

et al.

Current Obesity Reports, Journal Year: 2025, Volume and Issue: 14(1)

Published: Jan. 3, 2025

Language: Английский

Mechanisms controlling cellular and systemic iron homeostasis DOI
Bruno Galy, Marcus Conrad, Martina U. Muckenthaler

et al.

Nature Reviews Molecular Cell Biology, Journal Year: 2023, Volume and Issue: 25(2), P. 133 - 155

Published: Oct. 2, 2023

Language: Английский

Citations

290

Oxidative Stress in Liver Pathophysiology and Disease DOI Creative Commons
Abdolamir Allameh,

Reyhaneh Niayesh‐Mehr,

Azadeh Aliarab

et al.

Antioxidants, Journal Year: 2023, Volume and Issue: 12(9), P. 1653 - 1653

Published: Aug. 22, 2023

The liver is an organ that particularly exposed to reactive oxygen species (ROS), which not only arise during metabolic functions but also the biotransformation of xenobiotics. disruption redox balance causes oxidative stress, affects function, modulates inflammatory pathways and contributes disease. Thus, stress implicated in acute injury pathogenesis prevalent infectious or chronic diseases such as viral hepatitis B C, alcoholic fatty disease, non-alcoholic disease (NAFLD) steatohepatitis (NASH). Moreover, plays a crucial role progression fibrosis, cirrhosis hepatocellular carcinoma (HCC). Herein, we provide overview on effects pathophysiology mechanisms by promotes

Language: Английский

Citations

147

Inhibition of ferroptosis and iron accumulation alleviates pulmonary fibrosis in a bleomycin model DOI Creative Commons

Zhuo Pei,

Yifei Qin, Xianghui Fu

et al.

Redox Biology, Journal Year: 2022, Volume and Issue: 57, P. 102509 - 102509

Published: Oct. 18, 2022

Idiopathic pulmonary fibrosis (IPF) is a chronic progressive disease characterized by excessive proliferation of fibroblasts and accumulation extracellular matrix (ECM). Ferroptosis novel form cell death the lethal iron lipid peroxidation, which associated with many diseases. Our study addressed potential role played ferroptosis in progression fibrosis. We found that inducers injury, namely, bleomycin (BLM) lipopolysaccharide (LPS), induced lung epithelial cells. Both inhibitor liproxstatin-1 (Lip-1) chelator deferoxamine (DFO) alleviated symptoms or LPS. TGF-β stimulation upregulated expression transferrin receptor protein 1 (TFRC) human fibroblast line (MRC-5) mouse primary fibroblasts, resulting increased intracellular Fe2+, promoted transformation into myofibroblasts. Mechanistically, enhanced nuclear localization transcriptional coactivator tafazzin (TAZ), combined transcription factor TEA domain (TEAD)-4 to promote TFRC. In addition, elevated Fe2+ failed induce might be related regulation export metabolism. Finally, we specifically knocked out TFRC mice, compared those control were reduced knockout mice after induction. Collectively, these findings suggest therapeutic inhibitors chelators treating

Language: Английский

Citations

132

Iron metabolism and ferroptosis in type 2 diabetes mellitus and complications: mechanisms and therapeutic opportunities DOI Creative Commons
Runyu Miao, Xinyi Fang, Yanjiao Zhang

et al.

Cell Death and Disease, Journal Year: 2023, Volume and Issue: 14(3)

Published: March 8, 2023

Abstract The maintenance of iron homeostasis is essential for proper endocrine function. A growing body evidence suggests that imbalance a key factor in the development several diseases. Nowadays, ferroptosis, an iron-dependent form regulated cell death, has become increasingly recognized as important process to mediate pathogenesis and progression type 2 diabetes mellitus (T2DM). It been shown ferroptosis pancreas β cells leads decreased insulin secretion; liver, fat, muscle induces resistance. Understanding mechanisms concerning regulation metabolism T2DM may lead improved disease management. In this review, we summarized connection between metabolic pathways molecular T2DM. Additionally, discuss potential targets treating analysis current limitations future directions these novel treatment targets.

Language: Английский

Citations

85

Metabolic reprogramming in liver fibrosis DOI Creative Commons
Paul Horn, Frank Tacke

Cell Metabolism, Journal Year: 2024, Volume and Issue: 36(7), P. 1439 - 1455

Published: May 31, 2024

Chronic liver diseases, primarily metabolic dysfunction-associated steatotic disease (MASLD), harmful use of alcohol, or viral hepatitis, may result in fibrosis, cirrhosis, and cancer. Hepatic fibrogenesis is a complex process with interactions between different resident non-resident heterogeneous cell populations, ultimately leading to deposition extracellular matrix organ failure. Shifts phenotypes functions involve pronounced transcriptional protein synthesis changes that require adaptations cellular substrate metabolism, including glucose lipid resembling associated the Warburg effect cancer cells. Cell activation are regulated by stress responses, unfolded response, endoplasmic reticulum stress, autophagy, ferroptosis, nuclear receptor signaling. These crucial for inflammatory fibrogenic macrophages, lymphoid cells, hepatic stellate Modulation these pathways, therefore, offers opportunities novel therapeutic approaches halt even reverse fibrosis progression.

Language: Английский

Citations

67

The mechanism of ferroptosis and its related diseases DOI Creative Commons
Shijian Feng, Dan Tang, Yichang Wang

et al.

Molecular Biomedicine, Journal Year: 2023, Volume and Issue: 4(1)

Published: Oct. 16, 2023

Abstract Ferroptosis, a regulated form of cellular death characterized by the iron-mediated accumulation lipid peroxides, provides novel avenue for delving into intersection metabolism, oxidative stress, and disease pathology. We have witnessed mounting fascination with ferroptosis, attributed to its pivotal roles across diverse physiological pathological conditions including developmental processes, metabolic dynamics, oncogenic pathways, neurodegenerative cascades, traumatic tissue injuries. By unraveling intricate underpinnings molecular machinery, contributors, signaling conduits, regulatory networks governing researchers aim bridge gap between intricacies this unique mode multifaceted implications health disease. In light rapidly advancing landscape ferroptosis research, we present comprehensive review aiming at extensive in origins progress human diseases. This concludes careful analysis potential treatment approaches carefully designed either inhibit or promote ferroptosis. Additionally, succinctly summarized therapeutic targets compounds that hold promise targeting within various facet underscores burgeoning possibilities manipulating as strategy. summary, enriched insights both investigators practitioners, while fostering an elevated comprehension latent translational utilities. revealing basic processes investigating possibilities, crucial resource scientists medical aiding deep understanding effects situations.

Language: Английский

Citations

62

Consensus Statement on the definition and classification of metabolic hyperferritinaemia DOI Open Access
Luca Valenti, Elena Corradini, Leon A. Adams

et al.

Nature Reviews Endocrinology, Journal Year: 2023, Volume and Issue: 19(5), P. 299 - 310

Published: Feb. 17, 2023

Language: Английский

Citations

57

Found in translation—Fibrosis in metabolic dysfunction–associated steatohepatitis (MASH) DOI
Shuang Wang, Scott L. Friedman

Science Translational Medicine, Journal Year: 2023, Volume and Issue: 15(716)

Published: Oct. 4, 2023

Metabolic dysfunction–associated steatohepatitis (MASH) is a severe form of liver disease that poses global health threat because its potential to progress advanced fibrosis, leading cirrhosis and cancer. Recent advances in single-cell methodologies, refined models, genetic epigenetic insights have provided nuanced understanding MASH fibrogenesis, with substantial cellular heterogeneity livers providing potentially targetable cell-cell interactions behavior. Unlike mechanisms underlying fibrosis regression are still inadequately understood, although antifibrotic targets been recently identified. A treatment framework could lead noninvasive assessment targeted therapies preserve hepatocellular function restore the liver’s architectural integrity.

Language: Английский

Citations

55

Polyamine-mediated ferroptosis amplification acts as a targetable vulnerability in cancer DOI Creative Commons
Guoshu Bi, Jiaqi Liang, Yunyi Bian

et al.

Nature Communications, Journal Year: 2024, Volume and Issue: 15(1)

Published: March 19, 2024

Abstract Targeting ferroptosis, an iron-dependent form of regulated cell death triggered by the lethal overload lipid peroxides, in cancer therapy is impeded our limited understanding intersection tumour’s metabolic feature and ferroptosis vulnerability. In present study, arginine identified as a ferroptotic promoter using metabolites library. This effect mainly achieved through arginine’s conversion to polyamines, which exerts their potent ferroptosis-promoting property H 2 O -dependent manner. Notably, expression ornithine decarboxylase 1 (ODC1), critical enzyme catalysing polyamine synthesis, significantly activated signal——iron overload——through WNT/MYC signalling, well subsequent elevated thus forming ferroptosis-iron overload-WNT/MYC-ODC1-polyamine-H positive feedback loop that amplifies ferroptosis. Meanwhile, we notice cells release enhanced polyamine-containing extracellular vesicles into microenvironment, thereby further sensitizing neighbouring accelerating “spread” tumour region. Besides, supplementation also sensitizes or xenograft tumours radiotherapy chemotherapy inducing Considering are often characterized intracellular pools, results indicate metabolism exposes targetable vulnerability represents exciting opportunity for therapeutic strategies cancer.

Language: Английский

Citations

35

Exosome-Mediated Impact on Systemic Metabolism DOI Creative Commons

Karina Cunha e Rocha,

Wei Ying, Jerrold M. Olefsky

et al.

Annual Review of Physiology, Journal Year: 2024, Volume and Issue: 86(1), P. 225 - 253

Published: Feb. 12, 2024

Exosomes are small extracellular vesicles that carry lipids, proteins, and microRNAs (miRNAs). They released by all cell types can be found not only in circulation but many biological fluids. essential for interorgan communication because they transfer their contents from donor to recipient cells, modulating cellular functions. The miRNA content of exosomes is responsible most effects, changes exosomal levels contribute the progression or regression metabolic diseases. As miRNAs selectively sorted packaged into exosomes, useful as biomarkers diagnosing field metabolism expanding rapidly, researchers consistently making new discoveries this area. a result, have great potential next-generation drug delivery platform

Language: Английский

Citations

30