Alterations in the serum metabolome and proteome of adults after acclimatization to hypoxic environments at different altitudes DOI Creative Commons
Jiao Zhao, Weili Liu, Xiaoming Wang

et al.

Research Square (Research Square), Journal Year: 2024, Volume and Issue: unknown

Published: Dec. 2, 2024

Abstract Long-term exposure to high altitudes can induce adaptive or pathological changes in humans; however, the effects of altitude on human serum remain unclear. This study employed untargeted metabolomics and proteomics examine differences metabolites proteins from subjects residing at 2900, 3500, 4300, 4600 m for least one year compared with those a plain area (altitude 3 m) under normoxic conditions. The results revealed that long-term high-altitude hypoxia significantly altered proteins. Moreover, pathways linoleic acid metabolism, arachidonic (AA) complement coagulation cascades were response hypoxia. Further analysis extremely (3500–4600 promoted conversion AA into thromboxane A2, B2, 15(S)-hydroxyeicosatetraenoic acid, 12(S)-hydroxyeicosatetraenoic platelets, resulting reduced levels platelet aggregation. Additionally, metabolism platelets further increased increasing altitude. Exposure areas (2900–4600 meters) oxygen transport, glycolysis, coagulation, inhibits activation by expression such as globin, glyceraldehyde-3-phosphate dehydrogenase, superoxide dismutase 1, carbonate dehydratase II, inhibiting component 1q. inhibition fibrinogen factor XI may represent physiological thrombosis be associated liver injury. These findings indicate promotes adaptation transport interfering disrupts system inducing damage.

Language: Английский

LncRNA-HMG incites colorectal cancer cells to chemoresistance via repressing p53-mediated ferroptosis DOI Creative Commons

Zechang Xin,

Chen-Yu Hu,

Chunfeng Zhang

et al.

Redox Biology, Journal Year: 2024, Volume and Issue: 77, P. 103362 - 103362

Published: Sept. 18, 2024

Language: Английский

Citations

7
Role of glucose metabolic reprogramming in colorectal cancer progression and drug resistance DOI Creative Commons
Rong Qin, Xirui Fan, Yun‐Wen Huang

et al.

Translational Oncology, Journal Year: 2024, Volume and Issue: 50, P. 102156 - 102156

Published: Oct. 13, 2024

Language: Английский

Citations

4
JAK/STAT signaling as a key regulator of ferroptosis: mechanisms and therapeutic potentials in cancer and diseases DOI Creative Commons

Yimeng Dai,

Chunguo Cui,

Dan Jiao

et al.

Cancer Cell International, Journal Year: 2025, Volume and Issue: 25(1)

Published: March 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.

Language: Английский

Citations

0
The Dual Roles of STAT3 in Ferroptosis: Mechanism, Regulation and Therapeutic Potential DOI Creative Commons

Jinghui Xie,

Dan Luo, Pengfei Xing

et al.

Journal of Inflammation Research, Journal Year: 2025, Volume and Issue: Volume 18, P. 4251 - 4266

Published: March 1, 2025

Ferroptosis, an iron-dependent programmed mechanism of cell death that is driven by lipid peroxidation, important pathogenic factor in oncological and non-oncological disorders. Dysregulation iron metabolism profoundly influences disease progression through ferroptosis modulation. Signal transducer activator transcription 3 (STAT3), a transcriptional regulator, regulates binding to promoters key molecules such as solute carrier family 7 member 11 (SLC7A11), glutathione peroxidase 4 (GPX4), ferritin heavy chain 1 (FTH1). In this review, we described the role STAT3 supporting tumors survival suppressing malignancies, bidirectionally regulating non-tumors regulate development disease. We also reported emerging therapeutic strategies target STAT3-mediated ferroptosis, including natural phytochemicals, inhibitors, nanotechnology-enabled drug delivery systems. These advancements deepen mechanistic understanding regulation, provide new theoretical bases treat ferroptosis-related diseases.

Language: Английский

Citations

0
Emerging role of tumor microenvironmental nutrients and metabolic molecules in ferroptosis: Mechanisms and clinical implications DOI Open Access
Dongyu Li, Zhe Zhang, Lei Wang

et al.

Biomedicine & Pharmacotherapy, Journal Year: 2024, Volume and Issue: 179, P. 117406 - 117406

Published: Sept. 9, 2024

Language: Английский

Citations

2
Role of ENO1 and its targeted therapy in tumors DOI Creative Commons
Yafei Li, Lu Liu, Bo Li

et al.

Journal of Translational Medicine, Journal Year: 2024, Volume and Issue: 22(1)

Published: Nov. 14, 2024

ENO1, also called 2-phospho-D-glycerate hydrolase in cellular glycolysis, is an enzyme that converts 2-phosphoglycerate to phosphoenolpyruvate and plays important role the Warburg effect. In various tumors, ENO1 overexpression correlates with poor prognosis. a multifunctional oncoprotein that, when located on cell surface, acts as "moonlighting protein" promote tumor invasion metastasis. When intracellularly, facilitates glycolysis dysregulate energy sustain proliferation. Additionally, it promotes progression by activating oncogenic signaling pathways. biomarker represents promising target for therapy. This review summarizes recent advances from 2020 2024 understanding relationship between tumors explores latest targeted therapeutic strategies involving ENO1.

Language: Английский

Citations

1
Knockdown of ENO1 promotes autophagy dependent‐ferroptosis and suppresses glycolysis in breast cancer cells via the regulation of CST1 DOI Open Access
Guoliang Huang, Lian Lu,

Yuhong You

et al.

Drug Development Research, Journal Year: 2024, Volume and Issue: 85(7)

Published: Nov. 1, 2024

Autophagy-dependent ferroptosis and glycolysis play a significant role in tumor development. α-Enolase (ENO1), glycolytic enzyme, has been demonstrated to function as crucial modulator breast cancer (BC). However, the specific mechanism by which ENO1 influences of BC remains unclear. qRT-PCR, along with western blot analysis was applied investigate cystatin SN (CST1) expression cells. Glycolysis level measured extracellular acidification rate (ECAR), lactate production, glucose consumption, analysis. Ferroptosis evaluated iron lipid peroxidation assay, DCFH-DA staining, Immunofluorescence, together adopted for assessing cell autophagy mTOR signaling pathway. Cell apoptosis Ki67 were TUNEL immunohistochemistry, respectively. had abundant existence lines. silencing inhibited but promoted autophagy. In addition, inhibitor 3-MA reversed impacts on ferroptosis. Meanwhile, activator MHY1485 opposing effects Moreover, CST1 could be extensively found lines, its overexpression vivo experiments illustrated that deletion suppressed growth, increased rate, restrained proliferation, glycolysis, autophagy, well reducing signaling. To sum up, mediated utophagy-dependent cells regulating CST1.

Language: Английский

Citations

0
Alterations in the serum metabolome and proteome of adults after acclimatization to hypoxic environments at different altitudes DOI Creative Commons
Jiao Zhao, Weili Liu, Xiaoming Wang

et al.

Research Square (Research Square), Journal Year: 2024, Volume and Issue: unknown

Published: Dec. 2, 2024

Abstract Long-term exposure to high altitudes can induce adaptive or pathological changes in humans; however, the effects of altitude on human serum remain unclear. This study employed untargeted metabolomics and proteomics examine differences metabolites proteins from subjects residing at 2900, 3500, 4300, 4600 m for least one year compared with those a plain area (altitude 3 m) under normoxic conditions. The results revealed that long-term high-altitude hypoxia significantly altered proteins. Moreover, pathways linoleic acid metabolism, arachidonic (AA) complement coagulation cascades were response hypoxia. Further analysis extremely (3500–4600 promoted conversion AA into thromboxane A2, B2, 15(S)-hydroxyeicosatetraenoic acid, 12(S)-hydroxyeicosatetraenoic platelets, resulting reduced levels platelet aggregation. Additionally, metabolism platelets further increased increasing altitude. Exposure areas (2900–4600 meters) oxygen transport, glycolysis, coagulation, inhibits activation by expression such as globin, glyceraldehyde-3-phosphate dehydrogenase, superoxide dismutase 1, carbonate dehydratase II, inhibiting component 1q. inhibition fibrinogen factor XI may represent physiological thrombosis be associated liver injury. These findings indicate promotes adaptation transport interfering disrupts system inducing damage.

Language: Английский

Citations

0