The Glycobiology of Pulmonary Arterial Hypertension.
The Glycobiology of Pulmonary Arterial Hypertension.
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DOI：
10.3390/metabo12040316
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发表时间：
2022-04-01
期刊：
影响因子：
4.1
通讯作者：
Barnes, Jarrod Wesley
中科院分区：
文献类型：
--
作者：
Vang, Shia;Cochran, Phillip;Sebastian Domingo, Julio;Krick, Stefanie;Barnes, Jarrod Wesley
肺动脉高压（PAH）是一种病因复杂的进行性肺血管疾病。诊断后未接受治疗的 PAH 病例生存率较低。多项报告表明，特发性 PAH 或 IPAH 与代谢失调有关，包括一氧化氮 (NO) 生物利用度改变和葡萄糖代谢失调。 PAH 中的代谢变化可能调节肺血管细胞增殖增加、血管生成、细胞凋亡抵抗和血管收缩等多种过程。最近的报告强调了癌症和异丙肾上腺素代谢异常之间的相似性。特别是，增加的葡萄糖摄取和改变的葡萄糖利用率已被记录并与上述过程相关。我们是第一个报告葡萄糖代谢改变与糖基化变化之间联系的人。随后的报告强调了类似的发现，包括代谢改变和异常糖基化在 IPAH 发病机制中的潜在作用。这篇综述将详细介绍证明 PAH 代谢失调的研究结果，重点是糖生物学。此外，本报告将说明多环芳烃和癌症病理学的相似性，并强调研究人员在该领域探索的新发现。
Pulmonary arterial hypertension (PAH) is a progressive pulmonary vascular disease of complex etiology. Cases of PAH that do not receive therapy after diagnosis have a low survival rate. Multiple reports have shown that idiopathic PAH, or IPAH, is associated with metabolic dysregulation including altered bioavailability of nitric oxide (NO) and dysregulated glucose metabolism. Multiple processes such as increased proliferation of pulmonary vascular cells, angiogenesis, apoptotic resistance, and vasoconstriction may be regulated by the metabolic changes demonstrated in PAH. Recent reports have underscored similarities between metabolic abnormalities in cancer and IPAH. In particular, increased glucose uptake and altered glucose utilization have been documented and have been linked to the aforementioned processes. We were the first to report a link between altered glucose metabolism and changes in glycosylation. Subsequent reports have highlighted similar findings, including a potential role for altered metabolism and aberrant glycosylation in IPAH pathogenesis. This review will detail research findings that demonstrate metabolic dysregulation in PAH with an emphasis on glycobiology. Furthermore, this report will illustrate the similarities in the pathobiology of PAH and cancer and highlight the novel findings that researchers have explored in the field.
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