Metformin improves nonalcoholic fatty liver disease in db/db mice by inhibiting ferroptosis DOI
Teng Zhang,

Meng‐Yan Wang,

Guodong Wang

et al.

European Journal of Pharmacology, Journal Year: 2024, Volume and Issue: 966, P. 176341 - 176341

Published: Jan. 19, 2024

Language: Английский

The emerging role of ferroptosis in inflammation DOI Open Access

Yitian Sun,

Peng Chen,

Bingtao Zhai

et al.

Biomedicine & Pharmacotherapy, Journal Year: 2020, Volume and Issue: 127, P. 110108 - 110108

Published: March 29, 2020

Ferroptosis is a newly discovered type of cell death triggered by intracellular phospholipid peroxidation that morphologically, biologically and genetically distinct from other types death. classified as regulated necrosis more immunogenic than apoptosis. To date, compelling evidence indicates ferroptosis plays an important role in inflammation, several antioxidants functioning inhibitors have been shown to exert anti-inflammatory effects experimental models certain diseases. Our review provides overview the link between inflammation; better understanding mechanisms underlying inflammation may hasten development promising therapeutic strategies involving address inflammation.

Language: Английский

Citations

578

Inflammation and aging: signaling pathways and intervention therapies DOI Creative Commons
Xia Li, Chentao Li, Wanying Zhang

et al.

Signal Transduction and Targeted Therapy, Journal Year: 2023, Volume and Issue: 8(1)

Published: June 8, 2023

Abstract Aging is characterized by systemic chronic inflammation, which accompanied cellular senescence, immunosenescence, organ dysfunction, and age-related diseases. Given the multidimensional complexity of aging, there an urgent need for a systematic organization inflammaging through dimensionality reduction. Factors secreted senescent cells, known as senescence-associated secretory phenotype (SASP), promote inflammation can induce senescence in normal cells. At same time, accelerates immune resulting weakened function inability to clear cells inflammatory factors, creates vicious cycle senescence. Persistently elevated levels organs such bone marrow, liver, lungs cannot be eliminated leading damage aging-related Therefore, has been recognized endogenous factor elimination could potential strategy anti-aging. Here we discuss at molecular, cellular, organ, disease levels, review current aging models, implications cutting-edge single cell technologies, well anti-aging strategies. Since preventing alleviating diseases improving overall quality life are ultimate goals research, our highlights critical features mechanisms along with latest developments future directions providing theoretical foundation novel practical

Language: Английский

Citations

524

The multifaceted role of ferroptosis in liver disease DOI Creative Commons
Junyi Chen, Xiaopeng Li, Chaodong Ge

et al.

Cell Death and Differentiation, Journal Year: 2022, Volume and Issue: 29(3), P. 467 - 480

Published: Jan. 24, 2022

Ferroptosis is an iron-dependent form of non-apoptotic cell death characterized by excessive lipid peroxidation and associated with a plethora pathological conditions in the liver. Emerging evidence supports notion that dysregulated metabolic pathways impaired iron homeostasis play role progression liver disease via ferroptosis. Although molecular mechanisms which ferroptosis causes are poorly understood, several ferroptosis-associated genes have been implicated disease. Here, we review physiological processing nutrients, our current understanding metabolism, characteristics ferroptosis, regulate In addition, summarize pathogenesis disease, including injury, non-alcoholic steatohepatitis, fibrosis, cirrhosis, hepatocellular carcinoma. Finally, discuss therapeutic potential targeting for managing

Language: Английский

Citations

430

Targeting ferroptosis opens new avenues for the development of novel therapeutics DOI Creative Commons

Shumin Sun,

Jie Shen, Jianwei Jiang

et al.

Signal Transduction and Targeted Therapy, Journal Year: 2023, Volume and Issue: 8(1)

Published: Sept. 21, 2023

Abstract Ferroptosis is an iron-dependent form of regulated cell death with distinct characteristics, including altered iron homeostasis, reduced defense against oxidative stress, and abnormal lipid peroxidation. Recent studies have provided compelling evidence supporting the notion that ferroptosis plays a key pathogenic role in many diseases such as various cancer types, neurodegenerative disease, involving tissue and/or organ injury, inflammatory infectious diseases. Although precise regulatory networks underlie are largely unknown, particularly respect to initiation progression diseases, recognized bona fide target for further development treatment prevention strategies. Over past decade, considerable progress has been made developing pharmacological agonists antagonists these ferroptosis-related conditions. Here, we provide detailed overview our current knowledge regarding ferroptosis, its pathological roles, regulation during disease progression. Focusing on use chemical tools preclinical studies, also summarize recent advances targeting across growing spectrum ferroptosis-associated Finally, discuss new challenges opportunities potential strategy treating

Language: Английский

Citations

243

Ferritinophagy and ferroptosis in the management of metabolic diseases DOI
Amir Ajoolabady,

Hamid Aslkhodapasandhokmabad,

Peter Libby

et al.

Trends in Endocrinology and Metabolism, Journal Year: 2021, Volume and Issue: 32(7), P. 444 - 462

Published: May 15, 2021

Language: Английский

Citations

241

Cell Death in Liver Diseases: A Review DOI Open Access
Layla Shojaie, Andrea Iorga, Lily Dara

et al.

International Journal of Molecular Sciences, Journal Year: 2020, Volume and Issue: 21(24), P. 9682 - 9682

Published: Dec. 18, 2020

Regulated cell death (RCD) is pivotal in directing the severity and outcome of liver injury. Hepatocyte a critical event progression disease due to resultant inflammation leading fibrosis. Apoptosis, necrosis, necroptosis, autophagy, recently, pyroptosis ferroptosis, have all been investigated pathogenesis various diseases. These subroutines display distinct features, while sharing many similar characteristics with considerable overlap crosstalk. Multiple types modes can likely coexist, different populations may contribute injury each type disease. This review addresses known signaling cascades pathway its implications In this review, we describe common findings model, as well controversies limitations current data particular focus on death-related research humans rodent models alcoholic disease, non-alcoholic fatty steatohepatitis (NASH/NAFLD), acetaminophen (APAP)-induced hepatotoxicity, autoimmune hepatitis, cholestatic viral hepatitis.

Language: Английский

Citations

224

Interaction between macrophages and ferroptosis DOI Creative Commons
Yan Yang, Yu Wang, Lin Guo

et al.

Cell Death and Disease, Journal Year: 2022, Volume and Issue: 13(4)

Published: April 16, 2022

Abstract Ferroptosis, a newly discovered iron-dependent cell death pathway, is characterized by lipid peroxidation and GSH depletion mediated iron metabolism morphologically, biologically genetically different from other programmed deaths. Besides, ferroptosis usually found accompanied inflammatory reactions. So far, it has been participating in the development of many kinds diseases. Macrophages are group immune cells that widely exist our body for host defense play an important role tissue homeostasis mediating inflammation regulating iron, amino acid metabolisms through their unique functions like phagocytosis efferocytosis, cytokines secretion ROS production under polarization. According to these common points characteristics macrophages functions, it’s obvious there must be relationship between ferroptosis. Therefore, review aims at revealing interaction concerning three integrating application certain curing diseases, mostly cancer. Finally, we also provide inspirations further studies therapy some diseases targeting resident distinct tissues regulate Facts Ferroptosis considered as form its nonapoptotic hydroperoxide, metabolisms. playing crucial part various including hepatic neurological cancer, etc. phagocytic cells, existing owning such production. proved participate initiating reactions maintain balance body. Recent try treat cancer altering macrophages’ polarization which damages tumor microenvironment induces cells. Open questions How do specifically? Can use treating than cancer? What can related macrophages? Is more effective therapies when diseases?

Language: Английский

Citations

222

GPX4: The hub of lipid oxidation, ferroptosis, disease and treatment DOI
Yi Liu,

Yicong Wan,

Yi Jiang

et al.

Biochimica et Biophysica Acta (BBA) - Reviews on Cancer, Journal Year: 2023, Volume and Issue: 1878(3), P. 188890 - 188890

Published: March 29, 2023

Language: Английский

Citations

220

Targeted therapeutics and novel signaling pathways in non-alcohol-associated fatty liver/steatohepatitis (NAFL/NASH) DOI Creative Commons
Xiaohan Xu, Kyle L. Poulsen, Lijuan Wu

et al.

Signal Transduction and Targeted Therapy, Journal Year: 2022, Volume and Issue: 7(1)

Published: Aug. 13, 2022

Non-alcohol-associated fatty liver/steatohepatitis (NAFL/NASH) has become the leading cause of liver disease worldwide. NASH, an advanced form NAFL, can be progressive and more susceptible to developing cirrhosis hepatocellular carcinoma. Currently, lifestyle interventions are most essential effective strategies for preventing controlling NAFL without development fibrosis. While there still limited appropriate drugs specifically treat NAFL/NASH, growing progress is being seen in elucidating pathogenesis identifying therapeutic targets. In this review, we discussed recent developments etiology prospective targets, as well pharmacological candidates pre/clinical trials patents, with a focus on diabetes, hepatic lipid metabolism, inflammation, Importantly, evidence elucidates that disruption gut-liver axis microbe-derived metabolites drive NAFL/NASH. Extracellular vesicles (EVs) act signaling mediator, resulting accumulation, macrophage stellate cell activation, further promoting inflammation fibrosis progression during Targeting gut microbiota or EVs may serve new treatment Finally, other mechanisms, such therapy genetic approaches, also have enormous potential. Incorporating different mechanisms personalized medicine improve efficacy better benefit patients

Language: Английский

Citations

207

Changes in Glutathione Content in Liver Diseases: An Update DOI Creative Commons
Mariapia Vairetti, Laura Giuseppina Di Pasqua, Marta Cagna

et al.

Antioxidants, Journal Year: 2021, Volume and Issue: 10(3), P. 364 - 364

Published: Feb. 28, 2021

Glutathione (GSH), a tripeptide particularly concentrated in the liver, is most important thiol reducing agent involved modulation of redox processes. It has also been demonstrated that GSH cannot be considered only as mere free radical scavenger but it takes part network governing choice between survival, necrosis and apoptosis well altering function signal transduction transcription factor molecules. The purpose present review to provide an overview on molecular biology system; therefore, synthesis, metabolism regulation will reviewed. multiple functions described, importance compartmentalization into distinct subcellular pools inter-organ transfer. Furthermore, we highlight close relationship existing content pathogenesis liver disease, such non-alcoholic fatty disease (NAFLD), alcoholic (ALD), chronic cholestatic injury, ischemia/reperfusion damage, hepatitis C virus (HCV), B (HBV) hepatocellular carcinoma. Finally, potential therapeutic benefits GSH-related medications, described for each disorder taken account.

Language: Английский

Citations

198