The mechanism of ferroptosis and its related diseases

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

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Ferroptosis in immunostimulation and immunosuppression

Immunological Reviews, Journal Year: 2023, Volume and Issue: 321(1), P. 199 - 210

Published: July 9, 2023

Summary Ferroptosis is a form of iron‐dependent regulated cell death characterized by the accumulation toxic lipid peroxides, particularly in plasma membrane, leading to lytic death. While it plays crucial role maintaining overall health and proper functioning multicellular organisms, can also contribute tissue damage pathological conditions. Although ferroptotic generally recognized as an immunostimulatory process associated with release damage‐associated molecular patterns (DAMPs), occurrence ferroptosis immune cells or immunosuppressive molecules result tolerance. Consequently, there ongoing exploration targeting upstream signals machinery therapeutically enhance inhibit response. In addition introducing core mechanisms ferroptosis, we will focus on characteristics conditions, context infection, sterile inflammation, tumor immunity.

Language: Английский

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The Interplay between Ferroptosis and Neuroinflammation in Central Neurological Disorders

Antioxidants, Journal Year: 2024, Volume and Issue: 13(4), P. 395 - 395

Published: March 26, 2024

Central neurological disorders are significant contributors to morbidity, mortality, and long-term disability globally in modern society. These encompass neurodegenerative diseases, ischemic brain traumatic injury, epilepsy, depression, more. The involved pathogenesis is notably intricate diverse. Ferroptosis neuroinflammation play pivotal roles elucidating the causes of cognitive impairment stemming from these diseases. Given concurrent occurrence ferroptosis due metabolic shifts such as iron ROS, well their critical central nervous disorders, investigation into co-regulatory mechanism has emerged a prominent area research. This paper delves mechanisms along with interrelationship. It specifically emphasizes core molecules within shared pathways governing neuroinflammation, including SIRT1, Nrf2, NF-κB, Cox-2, iNOS/NO·, how different immune cells structures contribute dysfunction through mechanisms. Researchers’ findings suggest that mutually promote each other may represent key factors progression disorders. A deeper comprehension common pathway between cellular holds promise for improving symptoms prognosis related

Language: Английский

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The Multifaceted Roles of BACH1 in Disease: Implications for Biological Functions and Therapeutic Applications

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

Published: Jan. 30, 2025

Abstract BTB domain and CNC homolog 1 (BACH1) belongs to the family of basic leucine zipper proteins is expressed in most mammalian tissues. It can regulate its own expression play a role transcriptionally activating or inhibiting downstream target genes. has crucial various biological processes, such as oxidative stress, cell cycle, heme homeostasis, immune regulation. Recent research highlights BACH1's significant regulatory roles series conditions, including stem pluripotency maintenance differentiation, growth, senescence, apoptosis. BACH1 closely associated with cardiovascular diseases contributes angiogenesis, atherosclerosis, restenosis, pathological cardiac hypertrophy, myocardial infarction, ischemia/reperfusion (I/R) injury. promotes tumor proliferation metastasis by altering metabolism epithelial‐mesenchymal transition phenotype. Moreover, appears show an adverse neurodegenerative diseases, gastrointestinal disorders, leukemia, pulmonary fibrosis, skin diseases. Inhibiting may be beneficial for treating these This review summarizes mechanism different types proposing that precise targeted intervention provide new strategies human disease prevention treatment.

Language: Английский

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The role of ferroptosis in intervertebral disc degeneration

Frontiers in Cell and Developmental Biology, Journal Year: 2023, Volume and Issue: 11

Published: July 27, 2023

Nucleus pulposus, annulus fibrosus, and cartilage endplate constitute an avascular intervertebral disc (IVD), which is crucial for spinal joint mobility. As one of the most widespread health issues worldwide, degeneration (IVDD) recognized as a key contributor to back neck discomfort. A number degenerative disorders have strong correlation with ferroptosis, recently identified novel regulated cell death (RCD) characterized by iron-dependent mechanism buildup lipid reactive oxygen species (ROS). There growing interest in part ferroptosis plays IVDD pathophysiology. Inhibiting has been shown control development. Several studies demonstrated that TBHP-induced oxidative stress models, changes marker protein levels increased peroxidation lead cells, subsequently aggravates IVDD. Similarly, significantly relieved use inhibitors. The purpose this review was threefold: 1) discuss occurrence IVDD; 2) understand its role pathophysiology; 3) investigate feasibility prospect treatment.

Language: Английский

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Cr(VI) induces ferroptosis in DF-1 cells by simultaneously perturbing iron homeostasis of ferritinophagy and mitophagy

The Science of The Total Environment, Journal Year: 2024, Volume and Issue: 925, P. 171818 - 171818

Published: March 19, 2024

Language: Английский

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High-altitude hypoxia aggravated neurological deficits in mice induced by traumatic brain injury via BACH1 mediating astrocytic ferroptosis

Cell Death Discovery, Journal Year: 2025, Volume and Issue: 11(1)

Published: Feb. 5, 2025

Abstract Traumatic brain injury (TBI) is one of the leading causes disability and mortality, which was classified as low-altitude TBI high-altitude TBI. A large amount literature shows that associated with more severe neurological impairments higher mortality rates compared to TBI, due special environment hypoxia. However, role hypoxia in pathogenesis remains unclear. In order deeply investigate this scientific issue, we constructed a hypoxic model at different altitudes used animal behavioral assessments (Modified severity score, rotarod test, elevated plus maze test) well histopathological analyses (brain gross specimens, water content, Evans blue inducible factor-1α, Hematoxylin-Eosin staining ROS detection) reveal its underlying principles characteristics. We found altitude, TBI-induced deficits were changes significant. Single-nuclear RNA sequencing subsequently employed further differential gene expression profiles significant increase ferroptosis astrocytes cases those Analyzing transcription factors depth, Bach1 plays crucial regulating key molecules induce following Down-regulation can effectively alleviate mice. conclusion, may significantly enhance aggravate by up-regulating expression. Our study provides theoretical foundation for understanding mechanism targeted intervention therapy.

Language: Английский

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The potential roles of HIF-1α in epithelial-mesenchymal transition and ferroptosis in tumor cells

Cellular Signalling, Journal Year: 2024, Volume and Issue: 122, P. 111345 - 111345

Published: Aug. 10, 2024

In tumors, the rapid proliferation of cells and imperfect blood supply system lead to hypoxia, which can regulate adaptation tumor hypoxic environment through hypoxia-inducible factor-1α (HIF-1α) promote development in multiple ways. Recent studies have found that epithelial-mesenchymal transition (EMT) ferroptosis play important roles progression cells. The activation HIF-1α is considered a key factor inducing EMT When activated, it EMT-related genes, causing gradually lose their epithelial characteristics acquire more invasive mesenchymal traits. occurrence allows better adapt changes surrounding tissue, enhancing migratory capabilities, thus promoting progression. At same time, also plays crucial regulatory role environment, may affect processes such as iron metabolism oxidative stress responses, This article briefly reviews dual cells, helping gain deeper understanding pathways providing new perspective for pathogenesis tumors. regulation become an strategy future therapy.

Language: Английский

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Ferroptosis-based advanced therapies as treatment approaches for metabolic and cardiovascular diseases

Cell Death and Differentiation, Journal Year: 2024, Volume and Issue: 31(9), P. 1104 - 1112

Published: July 27, 2024

Ferroptosis has attracted attention throughout the last decade because of its tremendous clinical importance. Here, we review rapidly growing body literature on how inhibition ferroptosis may be harnessed for treatment common diseases, and focus metabolic cardiovascular unmet medical needs. We introduce four classes preclinically established inhibitors (ferrostatins) such as iron chelators, radical trapping agents that function in cytoplasmic compartment, lipophilic antioxidants ninjurin-1 (NINJ1) specific monoclonal antibodies. In contrast to inducers cause serious untoward effects acute kidney tubular necrosis, side effect profile ferrostatins appears limited. also consider a potential itself when several advanced therapies harnessing small-interfering RNA (siRNA)-based approaches are tested. Importantly, trial design is impeded by lack an appropriate biomarker detection serum samples or tissue biopsies. However, discuss favorable scenarios suited anti-ferroptosis trials test first-in-class compounds. conclude targeting exhibits outstanding options but have only begun translate this knowledge into clinically relevant applications.

Language: Английский

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Ferroptosis regulation by Cap’n’collar family transcription factors

Journal of Biological Chemistry, Journal Year: 2024, Volume and Issue: 300(8), P. 107583 - 107583

Published: July 16, 2024

Ferroptosis is an iron-dependent cell death mechanism that may be important to prevent tumor formation and useful as a target for new cancer therapies. Transcriptional networks play crucial role in shaping ferroptosis sensitivity by regulating the expression of transporters, metabolic enzymes, other proteins. The Cap'n'collar (CNC) protein nuclear factor erythroid 2 like (NFE2L2, also known NRF2) key regulator many cells contexts. Emerging evidence indicates related CNC family members BTB homology 1 (BACH1) (NFE2L1) have non-redundant roles regulation. Here, we comprehensively review transcription factors governing cellular ferroptosis. We describe how regulate through modulation iron, lipid, redox metabolism. use examples regulation proteins illustrate flexible highly context-dependent nature between conditions.

Language: Английский

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