Title : Pharmacologic ACE-Inhibition Mitigates Radiation-Induced Pneumonitis by Suppressing ACE-Expressing Lung Myeloid Cells.

Pub. Date : 2022 May 1

PMID : 35093482






8 Functional Relationships(s)
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1 Mitigation of radiation-induced pneumonitis with the ACE-inhibitor lisinopril was evaluated in the 13.5 Gy rat PBI model. Lisinopril angiotensin I converting enzyme Rattus norvegicus
2 Lisinopril abrogated radiation-induced increases in BALF MCP-1 (CCL2) and MIP-1alpha cytokine levels (p < 0.0001). Lisinopril C-C motif chemokine ligand 2 Homo sapiens
3 Lisinopril abrogated radiation-induced increases in BALF MCP-1 (CCL2) and MIP-1alpha cytokine levels (p < 0.0001). Lisinopril C-C motif chemokine ligand 2 Homo sapiens
4 Lisinopril abrogated radiation-induced increases in BALF MCP-1 (CCL2) and MIP-1alpha cytokine levels (p < 0.0001). Lisinopril C-C motif chemokine ligand 3 Homo sapiens
5 Treatment with lisinopril reduced both ACE expression (p=0.006) and frequency of CD45+CD11b+ lung myeloid cells (p=0.004). Lisinopril angiotensin I converting enzyme Homo sapiens
6 Treatment with lisinopril reduced both ACE expression (p=0.006) and frequency of CD45+CD11b+ lung myeloid cells (p=0.004). Lisinopril integrin subunit alpha M Homo sapiens
7 In vitro, radiation injury acutely increased ACE activity (p=0.045) and reactive oxygen species (ROS) generation (p=0.004) in human monocytes, whereas treatment with lisinopril blocked radiation-induced increases in both ACE and ROS. Lisinopril angiotensin I converting enzyme Homo sapiens
8 In vitro, radiation injury acutely increased ACE activity (p=0.045) and reactive oxygen species (ROS) generation (p=0.004) in human monocytes, whereas treatment with lisinopril blocked radiation-induced increases in both ACE and ROS. Lisinopril angiotensin I converting enzyme Homo sapiens