Pathology - Research and Practice, Journal Year: 2024, Volume and Issue: 254, P. 155134 - 155134
Published: Jan. 14, 2024
Language: Английский
Pathology - Research and Practice, Journal Year: 2024, Volume and Issue: 254, P. 155134 - 155134
Published: Jan. 14, 2024
Language: Английский
Life Sciences, Journal Year: 2024, Volume and Issue: 345, P. 122613 - 122613
Published: April 4, 2024
Language: Английский
Citations
25Chemico-Biological Interactions, Journal Year: 2024, Volume and Issue: 394, P. 111002 - 111002
Published: April 9, 2024
Lung inflammatory disorders are a major global health burden, impacting millions of people and raising rates morbidity death across many demographic groups. An industrial chemical common environmental contaminant, formaldehyde (FA) presents serious concerns to the respiratory system, including onset aggravation lung disorders. Epidemiological studies have shown significant associations between FA exposure levels incidence severity several diseases. causes inflammation in tract via immunological activation, oxidative stress, airway remodelling, aggravating pre-existing pulmonary compromising function. Additionally, functions as sensitizer, causing allergic responses hypersensitivity pneumonitis sensitive people. Understanding complicated processes behind formaldehyde-induced is critical for directing targeted strategies aimed at minimizing exposures alleviating burden formaldehyde-related illnesses on health. This abstract explores intricate relationship diseases, asthma, bronchitis, inflammation, injury fibrosis.
Language: Английский
Citations
22Biogerontology, Journal Year: 2025, Volume and Issue: 26(2)
Published: Feb. 26, 2025
Abstract Cellular senescence and hypoxia-inducible factor (HIF) signaling are crucial in pulmonary aging age-related lung diseases such as chronic obstructive disease idiopathic fibrosis cancer. HIF plays a pivotal role cellular adaptation to hypoxia, regulating processes like angiogenesis, metabolism, inflammation. Meanwhile, leads irreversible cell cycle arrest, triggering the senescence-associated secretory phenotype which contributes inflammation, tissue remodeling, fibrosis. Dysregulation of these pathways accelerates progression by promoting oxidative stress, mitochondrial dysfunction, epigenetic alterations. Recent studies indicate that interact at multiple levels, where can both induce suppress senescence, depending on conditions. While transient activation supports repair stress resistance, dysregulation exacerbates pathologies. Furthermore, emerging evidence suggests targeting could offer new therapeutic strategies mitigate diseases. This review explores intricate crosstalk between mechanisms, shedding light how their interplay influences progression. Additionally, we discuss potential interventions, including senolytic therapies modulators, enhance health longevity.
Language: Английский
Citations
2Clinica Chimica Acta, Journal Year: 2024, Volume and Issue: 565, P. 119983 - 119983
Published: Oct. 3, 2024
Language: Английский
Citations
15Ageing Research Reviews, Journal Year: 2024, Volume and Issue: 98, P. 102327 - 102327
Published: May 10, 2024
Language: Английский
Citations
14Pathology - Research and Practice, Journal Year: 2024, Volume and Issue: 256, P. 155259 - 155259
Published: March 11, 2024
Language: Английский
Citations
12Pathology - Research and Practice, Journal Year: 2024, Volume and Issue: 260, P. 155424 - 155424
Published: June 20, 2024
Language: Английский
Citations
10Pathology - Research and Practice, Journal Year: 2024, Volume and Issue: 256, P. 155257 - 155257
Published: March 13, 2024
Language: Английский
Citations
9Life Sciences, Journal Year: 2024, Volume and Issue: 344, P. 122576 - 122576
Published: March 14, 2024
Language: Английский
Citations
9Clinical and Experimental Medicine, Journal Year: 2024, Volume and Issue: 24(1)
Published: Sept. 26, 2024
Abstract Long non-coding RNAs (lncRNAs) have emerged as crucial regulators in various cellular processes, including cancer progression and stress response. Recent studies demonstrated that copper accumulation induces a unique form of cell death known cuproptosis, with lncRNAs playing key role regulating cuproptosis-associated pathways. These may trigger cell-specific responses to stress, presenting new opportunities prognostic markers therapeutic targets. This paper delves into the cuproptosis-mediated cancer, underscoring their potential biomarkers targets for innovative strategies. A thorough review scientific literature was conducted, utilizing databases such PubMed, Google Scholar, ScienceDirect, search terms like 'lncRNAs,' 'cuproptosis,' 'cancer.' Studies were selected based on relevance lncRNA regulation cuproptosis pathways implications prognosis treatment. The highlights significant contribution cuproptosis-related genes pathways, impacting metabolism, mitochondrial responses, apoptotic signaling. Specific are breast, lung, liver, ovarian, pancreatic, gastric cancers. objective this article is explore cancers mediated by cuproptosis.
Language: Английский
Citations
9