
Journal of Stroke and Cerebrovascular Diseases, Год журнала: 2024, Номер 34(2), С. 108205 - 108205
Опубликована: Дек. 18, 2024
Язык: Английский
Journal of Stroke and Cerebrovascular Diseases, Год журнала: 2024, Номер 34(2), С. 108205 - 108205
Опубликована: Дек. 18, 2024
Язык: Английский
Journal of Biochemical and Molecular Toxicology, Год журнала: 2025, Номер 39(1)
Опубликована: Янв. 1, 2025
ABSTRACT The eye is considered to be an immune‐privileged region. However, several parts of the have distinct mechanisms for delivering immune cells injury sites or even in response aging. Although these responses are intended protective, visual acuity can compromised by release pro‐inflammatory cytokines cells, which induce chronic inflammation and fibrosis. Age‐related diseases (AREDs) primary cause vision impairment (VI) elderly, with a poor comprehension their pathophysiology. affect both anterior posterior segments, resulting diminished quality life risk irreversible blindness. Immune system dysregulation upregulation been linked AREDs, underscoring need comprehend inflammation's impact on ocular disorders enhance patient symptom management. In this framework, PubMed database was searched using medical subject headings (MeSH) terms “Age‐related diseases,” “dry syndrome,” “glaucoma,” “cataract,” “diabetic retinopathy,” “inflammation,” “interleukin,” “cytokine” aim overview role AREDs discuss potential therapeutic approaches.
Язык: Английский
Процитировано
0International Journal of Molecular Sciences, Год журнала: 2025, Номер 26(3), С. 916 - 916
Опубликована: Янв. 22, 2025
Polychlorinated biphenyls (PCBs) are heterogeneous, synthetic, and widespread organochlorine compounds, one of the persistent organic pollutants present in improperly dumped waste electronic equipment (e-waste), with a high bioaccumulation potential. In this study, toxicity Aroclor 1254 (a mixture commercial PCBs) human corneal epithelial cells (HCEpiCs), an vitro model ocular barrier, was evaluated. (0.1–10 μg/mL) reduced cell viability, trans-endothelial electric resistance (TEER) migration. Moreover, it induced inflammatory response, as indicated by increase cPLA2 activity, PGE2 production, phosphorylation ERK 1/2 p-38, release cytokines. can damage cells, compromising integrity eye’s outermost barrier. This may facilitate occurrence infectious processes that physiologically prevented
Язык: Английский
Процитировано
0Naunyn-Schmiedeberg s Archives of Pharmacology, Год журнала: 2025, Номер unknown
Опубликована: Март 1, 2025
Язык: Английский
Процитировано
0International Immunopharmacology, Год журнала: 2024, Номер 139, С. 112678 - 112678
Опубликована: Июль 27, 2024
Язык: Английский
Процитировано
2Investigative Ophthalmology & Visual Science, Год журнала: 2024, Номер 65(5), С. 21 - 21
Опубликована: Май 13, 2024
Aging is a risk factor for dry eye. We sought to identify changes in the aged mouse corneal epithelial transcriptome and determine how age affects sensitivity, re-epithelialization, barrier reformation after debridement.
Язык: Английский
Процитировано
2medRxiv (Cold Spring Harbor Laboratory), Год журнала: 2024, Номер unknown
Опубликована: Сен. 8, 2024
Abstract Objective To investigate the roles of chemokines in activating NF-κB signaling pathway retinal pigment epithelium (RPE) and photoreceptor cells, their contribution to pathogenesis age-related macular degeneration (AMD). Background AMD is a leading cause vision loss older adults, driven by chronic inflammation oxidative stress. The transcription factor plays key role regulating these processes, with various chemokines, such as CCL2 CX3CL1, influencing activation. Despite advances treatment, deeper understanding how affect activation RPE cells remains critical for developing effective therapies. This study seeks address this gap improve management. Methods A comprehensive search databases, including PubMed, MEDLINE, Google Scholar, was conducted identify relevant studies on cells. covered (MCP-1), CX3CL1 (Fractalkine), CCL3 (MIP-1α), CCL5 (RANTES), CXCL8 (IL-8), CXCL10 (IP-10), CXCL1 (GRO-α), CXCL12 (SDF-1), CCL11 (Eotaxin), CXCL16, CXCL9 (MIG), CXCL11 (I-TAC). Studies were systematically reviewed following PRISMA guidelines assess involvement Results analysis revealed that CCL2, CCL3, CCL5, significantly activated increased apoptosis through enhanced cytokine production reactive oxygen species (ROS) generation. Additionally, CXCL8, CXCL10, CXCL1, triggered activation, contributing stress extracellular matrix (ECM) remodeling, which disrupts structure function. Other CCL11, CXCL9, CXCL11, sustained modulated metalloproteinases (MMPs), further implicating them progression. Conclusion Chemokines, CXCL12, activate driving inflammation, stress, ECM remodeling AMD. These findings highlight potential therapeutic targets mitigate disease
Язык: Английский
Процитировано
0Journal of Stroke and Cerebrovascular Diseases, Год журнала: 2024, Номер 34(2), С. 108205 - 108205
Опубликована: Дек. 18, 2024
Язык: Английский
Процитировано
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