md_a
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- Aug 31, 2015
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Serotonin (5-hydroxytryptamine; 5-HT) is known to increase proliferation and collagen synthesis by fibroblasts. Two receptor subtypes, 5-HT2A and 5-HT2B, have been shown to play the most important roles in the lung.
In conclusion, the present study has demonstrated the antifibrotic effect of specific serotonin 5-HT2A and 5-HT2B receptor antagonists in vivo using the animal model of bleomycin-induced lung fibrosis, and the involvement of the transforming growth factor-β1, connective growth factor and plasminogen activator inhibitor-1 pathways. The observations in human samples support the hypothesis that the serotonin pathway might be involved in the pathophysiology of human lung fibrosis.
Modulation of bleomycin-induced lung fibrosis by serotonin receptor antagonists in mice
Several viral proteins have been reported to modulate TGF-ß1 signaling, which could induce the proliferation of fibroblasts [25]. Pang et al [27] found higher serum concentrations of TGF-ß1 in SARS patients compared to controls for all clinical courses, including initial, peak, remission, and recovery stages [26,27]. During short-term follow-up, persistent ground glass opacities, reticular opacities, and pathologic findings of fibrosis have been found in some SARS survivors [28,29]. ...
... Willis et al [30] pointed out that TGF-ß1 was necessary but not sufficient to induce the formation of pulmonary fibrosis [30]. In our study, TGF-ß1 levels increased significantly and remained high after treatment in the severe group, coinciding with reports of patients with SARS-CoV infection [23,26]. This phenomenon could well be explained by the existence of imminent pulmonary fibrosis. ...
https://www.researchgate.net/public...dulates_Transforming_Growth_Factor-_Signaling
Losartan an angiotensin receptor blocker (ARB), also may lead to protection of lung fibrosis through other molecular mechanisms such as downregulation of TGF-β1.
Cinanserin, serotonin antagonists, the benefits of this is from its 5-HT2 antagonism.
The molecule is an inhibitor of the 3C-like protease of SARS-coronavirus (SARS)
Cinanserin - Wikipedia
In conclusion, the present study has demonstrated the antifibrotic effect of specific serotonin 5-HT2A and 5-HT2B receptor antagonists in vivo using the animal model of bleomycin-induced lung fibrosis, and the involvement of the transforming growth factor-β1, connective growth factor and plasminogen activator inhibitor-1 pathways. The observations in human samples support the hypothesis that the serotonin pathway might be involved in the pathophysiology of human lung fibrosis.
Modulation of bleomycin-induced lung fibrosis by serotonin receptor antagonists in mice
Several viral proteins have been reported to modulate TGF-ß1 signaling, which could induce the proliferation of fibroblasts [25]. Pang et al [27] found higher serum concentrations of TGF-ß1 in SARS patients compared to controls for all clinical courses, including initial, peak, remission, and recovery stages [26,27]. During short-term follow-up, persistent ground glass opacities, reticular opacities, and pathologic findings of fibrosis have been found in some SARS survivors [28,29]. ...
... Willis et al [30] pointed out that TGF-ß1 was necessary but not sufficient to induce the formation of pulmonary fibrosis [30]. In our study, TGF-ß1 levels increased significantly and remained high after treatment in the severe group, coinciding with reports of patients with SARS-CoV infection [23,26]. This phenomenon could well be explained by the existence of imminent pulmonary fibrosis. ...
https://www.researchgate.net/public...dulates_Transforming_Growth_Factor-_Signaling
Losartan an angiotensin receptor blocker (ARB), also may lead to protection of lung fibrosis through other molecular mechanisms such as downregulation of TGF-β1.
Cinanserin, serotonin antagonists, the benefits of this is from its 5-HT2 antagonism.
The molecule is an inhibitor of the 3C-like protease of SARS-coronavirus (SARS)
Cinanserin - Wikipedia
