Unraveling ferroptosis in osteogenic lineages: implications for dysregulated bone remodeling during periodontitis progression

Cell Death Discovery, Год журнала: 2024, Номер 10(1)

Опубликована: Апрель 26, 2024

Periodontitis is a highly prevalent disease characterized by inflammation and destruction of tooth-supporting tissues that leads to tooth loss in extreme situations. Elucidating the underlying mechanisms periodontitis pathogenesis progression will establish groundwork for developing effective treatment strategies. Recently, evidence concerning role ferroptosis has emerged. Osteogenic lineage cells are key regulators bone remodeling. cell death, as observed experimental models, disrupts balance between resorption formation. However, whether osteogenic undergoes during corresponding effect on remain elusive. Here, we investigated cell-specific within alveolar murine model. Through immunofluorescence double staining immunohistochemistry, identified ferroptotic osteocytes osteoblasts inflammatory bone. Next, vivo administration erastin or liproxstatin-1 was conducted either induce inhibit ferroptosis, respectively. Severe inflammation, accompanied increased osteoclast formation impaired potential were detected following activation. Subsequently, carried out vitro experiments further verified enhanced osteocytic expression RANKL IL-6. These findings suggest occurring acts catalyst stimulating osteoclastogenesis through secretion cytokines inhibiting osteoblastic function, providing insights into ferroptosis-induced alterations microenvironment-based intercellular communication. Ferroptosis promising target controlling preventing periodontitis.

Язык: Английский

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ALDH2 alleviates inflammation and facilitates osteogenic differentiation of periodontal ligament stem cells in periodontitis by blocking ferroptosis via activating Nrf2

Functional & Integrative Genomics, Год журнала: 2024, Номер 24(5)

Опубликована: Окт. 1, 2024

Язык: Английский

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Bomidin attenuates inflammation of periodontal ligament stem cells and periodontitis in mice via inhibiting ferroptosis

International Immunopharmacology, Год журнала: 2023, Номер 127, С. 111423 - 111423

Опубликована: Дек. 22, 2023

Язык: Английский

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Pre-treated Mesenchymal Stem Cell-Derived Exosomes: A New Perspective for Accelerating Spinal Cord Injury Repair

European Journal of Pharmacology, Год журнала: 2025, Номер 992, С. 177349 - 177349

Опубликована: Фев. 5, 2025

Spinal cord injury (SCI) is a devastating event for the central nervous system (CNS), often resulting in loss of sensory and motor functions. It profoundly affects both physiological psychological well-being patients, reducing their quality life while also imposing significant economic pressure on families healthcare system. Due to complex pathophysiology SCI, effective treatments promoting recovery remain scarce. Mesenchymal stem cell-derived exosomes (MSC-Exos) offer advantages such as low immunogenicity, good biocompatibility, ability cross blood-spinal barrier (BSCB). In preclinical studies, they have progressively shown efficacy SCI repair functional recovery. However, yield insufficient targeting MSC-Exos limit therapeutic efficacy. Currently, genetic engineering other preprocessing techniques are being employed optimize properties exosomes, thereby enhancing potential. Therefore, this paper provides an overview biogenesis exosomes. summarizes current approaches optimizing exosome performance. Additionally, it details mechanisms through which optimized provide neuroprotection explores potential combined involving hydrogels.

Язык: Английский

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4-Octyl Itaconate Attenuates Postmenopausal Osteoporosis by Inhibiting Ferroptosis and Enhancing Osteogenesis via the Nrf2 Pathway

Inflammation, Год журнала: 2025, Номер unknown

Опубликована: Фев. 22, 2025

Bone marrow mesenchymal stem cells (BMSCs) play an important role in bone metabolism and tissue repair, their ability to differentiate into osteoblasts is crucial the treatment of diseases such as postmenopausal osteoporosis (PMOP). However, function BMSCs may be affected by ferroptosis. Ferroptosis a cell death mode characterized excess Fe2+ lipid peroxidation, which significantly affects survival rate differentiation BMSCs. This study investigated effect exogenous itaconate derivative 4-octyl (4-OI) on Erastin-induced The results showed that 4-OI inhibited ferroptosis activating nuclear factor erythroid 2-related 2 (Nrf2) signaling pathway, reduced reactive oxygen species levels oxidative damage, restored antioxidant capacity. At same time, promoted osteogenic Further experiments Nrf2-IN-1, inhibitor Nrf2 could reverse protective 4-OI. In vivo, was shown reduce loss ovariectomized (OVX) mice, assessed Micro-CT analysis. Immunofluorescence staining further revealed increased GPX4 expression vertebral tissues following treatment. These indicate improves enhances providing new research ideas potential targets for PMOP.

Язык: Английский

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Ferroptosis and cuproptosis in periodontitis: recent biological insights and therapeutic advances

Frontiers in Immunology, Год журнала: 2025, Номер 16

Опубликована: Фев. 24, 2025

Periodontitis is a significant global public health issue associated with the onset and progression of various systemic diseases, thereby requiring additional research clinical attention. Although ferroptosis cuproptosis have emerged as areas in medical field, their precise roles pathogenesis periodontitis remain unclear. We aim to systematically summarize current on periodontal disease investigate glutathione pathway autophagy connecting during periodontitis. Further, we propose that homeostatic imbalance copper iron, driven by pathogens, may contribute elevated oxidative stress, representing potential unifying link between involved This article presents comprehensive overview molecular mechanisms underlying periodontitis, offering novel theoretical insights into its therapeutic targets.

Язык: Английский

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JAK/STAT signaling as a key regulator of ferroptosis: mechanisms and therapeutic potentials in cancer and diseases

Cancer Cell International, Год журнала: 2025, Номер 25(1)

Опубликована: Март 7, 2025

Ferroptosis is a distinct form of regulated cell death characterized by iron-dependent lipid peroxidation, playing critical role in various diseases, including cancer, neurodegeneration, and tissue damage. This study reviews the intricate relationship between ferroptosis Janus kinase/signal transducer activator transcription (JAK/STAT) signaling pathway, highlighting its regulatory functions across multiple biological processes. Dysregulation JAK/STAT pathway implicated promoting or inhibiting ferroptosis, depending on context. JAK2 promotes activating STAT proteins, modulating expression key regulators like SLC7A11 GPX4, influencing iron homeostasis through pathways such as ferritinophagy hepcidin regulation. STAT1 activation primarily enhances suppression cystine-glutamate antiporter (System Xc-), leading to glutathione depletion contributing conditions Sjogren's syndrome age-related macular degeneration. In contrast, STAT3 plays protective upregulating which inhibits survival, particularly cancers hepatocellular carcinoma, prostate renal carcinoma. also discusses STAT6's involvement diseases asthma lung injury regulating antioxidant defenses. Furthermore, review explores potential therapeutic strategies targeting manipulate for disease treatment. cancer therapy, this can enhance effectiveness inducers, offering promising avenues overcome drug resistance. Additionally, interplay immune responses, oxidative stress, metabolism underscores significance progression intervention. By exploring these mechanisms, provides insights into development novel treatments modulation, with implications inflammatory neurodegenerative conditions.

Язык: Английский

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Focusing on ferroptosis in alveolar bone loss during periodontitis: From mechanisms to therapies

International Immunopharmacology, Год журнала: 2025, Номер 156, С. 114683 - 114683

Опубликована: Апрель 18, 2025

Язык: Английский

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Bone Marrow Mesenchymal Stem Cell-Derived Exosomes Promote the Recovery of Spinal Cord Injury and Inhibit Ferroptosis by Inactivating IL-17 Pathway

Journal of Molecular Neuroscience, Год журнала: 2024, Номер 74(2)

Опубликована: Март 27, 2024

Язык: Английский

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Research progress on the regulatory cell death of osteoblasts in periodontitis

Journal of Zhejiang University (Medical Sciences), Год журнала: 2024, Номер 53(5), С. 533 - 540

Опубликована: Окт. 1, 2024

Periodontitis is a chronic inflammatory disease characterized by progressive destruction of alveolar bone. The most critical mechanism underlying bone the imbalance homeostasis, where osteoblast-mediated matrix synthesis plays an important role in regulating homeostasis. Regulated cell death instrumental both microenvironment and regulation Chronic inflammation, oxidative stress, other factors can be directly involved mitochondrial receptor-mediated signaling pathways, modulating B-cell lymphoma 2 family proteins cysteine aspartic acid specific protease (caspase) activity, thereby affecting osteoblast apoptosis inflammation cellular damage induce necroptosis via RIPK1/RIPK3/MLKL pathway, exacerbating response accelerating destruction. Stimuli such as pathogenic microorganisms injury may also activate caspase-1-dependent or independent pathways gasdermin D proteins, promoting pyroptosis releasing pro-inflammatory cytokines to mediate damage. Iron overload lipid peroxidation periodontitis trigger ferroptosis osteoblasts, impacting their survival function, ultimately leading homeostasis imbalance. This article focuses on periodontal through regulatory death, aiming provide research evidence for treatment

Язык: Английский

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