| تعداد نشریات | 284 |
| تعداد نشریات سازمان | 82 |
| تعداد شماره‌ها | 3,081 |
| تعداد مقالات | 34,371 |
| تعداد مشاهده مقاله | 47,878,264 |
| تعداد دریافت فایل اصل مقاله | 78,877,407 |
Angiotensin II-hnRNP K-VEGF Pathway: A Proposed Mechanism for Plasma Leakage in Dengue Virus Infection - A Narrative Review | ||
| Archives of Razi Institute | ||
| مقالات آماده انتشار، پذیرفته شده، انتشار آنلاین از تاریخ 13 مهر 1404 اصل مقاله (458.29 K) | ||
| نوع مقاله: Review Article | ||
| شناسه دیجیتال (DOI): 10.22092/ari.2025.370333.3782 | ||
| نویسندگان | ||
| Safari Wahyu Jatmiko* 1، 2؛ Riandini Aisyah1، 2؛ Restu Triwulandani Tolibin2، 3؛ Dini Amalia Firdausy1؛ Khansa Annora Amirinda1 | ||
| 1Department of Biomedical Science, Faculty of Medicine, Universitas Muhammadiyah Surakarta (UMS), Sukoharjo, Indonesia. | ||
| 2Tropical Diseases Research Group, Family Medicine Research Center, Faculty of Medicine, Universitas Muhammadiyah Surakarta (UMS), Sukoharjo, Indonesia. | ||
| 3Department of Clinical Science, Faculty of Medicine, Universitas Muhammadiyah Surakarta (UMS), Sukoharjo, Indonesia. | ||
| چکیده | ||
| Dengue virus infection (DVI) remains a global burden with increasing cases, deaths, and expansion of endemic areas. Plasma leakage (PL) as a major complication triggered by an immune response to DENV, but the molecular mechanism of increased vascular permeability has not been fully revealed. The hypothesis of the Angiotensin II (Ang II) – Heterogenous Nuclear Ribonucleoprotein K (hnRNP K) – Vascular Endothelial Growth Factor (VEGF) pathway is proposed as a key to the pathogenesis of PL. The aim of the paper is to review the scientific literature concerning the elements of the Ang II–hnRNP K–VEGF pathway, evaluate its association with PL in DVI, and develop a molecular hypothesis for future experimental research. Narrative review was conducted following Scale for Assessment of Narrative Review Articles (SANRA) guidelines. Literature search on PubMed, Scopus, ScienceDirect, and Google Scholar with keywords used alone or in combination as follows “dengue”, "dengue infection", "dengue Virus", "Angiotensin II", "Ang II", “hnRNPK”, "Heterogenous Nuclear Ribonucleoprotein K", "hnRNP K", "plasma leakage", "Vascular Leakage", "Vascular Permeability", "Capillary Leak Syndrome". The inclusion criteria are English-language articles published between 2000-2025, while grey literature was left out from the source literature. Based on the results of the review search, it was found that Ang II increased in severe dengue that activated PKCδ. PKCδ phosphorylates hnRNP K on Ser302 residues so that hnRNP K translocate to the cytoplasm and binds to VEGF mRNA. It stabilizes the mRNA & enhances VEGF translation. VEGF interacts with VEGFR2 in endothelial cells, thus activating FAK, TSAd/Src, and PI3K/Akt signaling pathways that cause phosphorylation of VE-cadherin and decreased VE-cadherin expression through nitric oxide production, triggering disruption of intercellular connections. This triggers an increase in vascular hyperpermeability leading to PL. Based on this, the Ang II–hnRNP K–VEGF pathway is a strong hypothesis of the cause of PL in DVI. In vivo experimental validation is required to confirm this mechanism. Pathway modulation (e.g., Ang II inhibitors such as losartan) has the potential to be a novel targeted therapy to prevent severe DVI progressivity and reduce mortality. | ||
| کلیدواژه‌ها | ||
| Dengue virus؛ Plasma leakage؛ Angiotensin II؛ hnRNP K؛ VEGF | ||
|
آمار تعداد مشاهده مقاله: 47 تعداد دریافت فایل اصل مقاله: 36 |
||