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- W2913202218 abstract "Rationale: Pulmonary arterial hypertension (PAH) is a vascular remodeling disease with a poor prognosis and no therapeutic option. It is now established that excessive proliferation and resistance to apoptosis of pulmonary artery smooth muscle cells (PASMCs) is a pivotal component of pulmonary vascular remodelling. Given that PAH and cancer cells share numerous similarities, this opens the possibility of exploiting therapeutic agents used in cancer to treat PAH. Cancer cells presenting intrinsic elevated replication stress (RS) rely on activation of the DNMT-1/miR-424/CHK1 pathway to restrain the accumulation of deleterious levels of DNA damage. CHK1 activation results in cell cycle arrest, DNA repair and finally, when stress is resolved, allows replication to resume. Objective: We hypothesize that PAH-PASMCs have developed an orchestrated response mediated by CHK1 to overcome RS/DNA damage, allowing survival and proliferation and thus contributing to vascular remodeling. Methods and Results: Using Wester..." @default.
- W2913202218 created "2019-02-21" @default.
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- W2913202218 date "2017-11-14" @default.
- W2913202218 modified "2023-09-23" @default.
- W2913202218 title "Abstract 17416: The DNMT-1/miR-424-Dependant Upregulation of CHK1 in PAH-PASMCs is Essential for Proliferation and Survival by Preventing Excessive Replication Stress" @default.
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