Dysregulation of BMP9/BMPR2/SMAD signalling pathway contributes to pulmonary fibrosis and pulmonary hypertension induced by bleomycin in rats
Background and Purpose Pulmonary hypertension related to pulmonary fibrosis is classed as WHO Group III, one of the most common groups which lacks effective treatment options. In this study, we aimed to uncover the underlying mechanisms, particularly the involvement of the BMP9/BMPR2/SMAD signalling...
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| Veröffentlicht in: | British journal of pharmacology 2021-01, Vol.178 (1), p.203-216 |
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| creator | Jiang, Qian Liu, Chunli Liu, Shiyun Lu, Wenju Li, Yi Luo, Xiaoyun Ma, Ran Zhang, Chenting Chen, Haixia Chen, Yuqin Zhang, Zizhou Hong, Cheng Guo, Wenliang Wang, Tao Yang, Kai Wang, Jian |
| description | Background and Purpose
Pulmonary hypertension related to pulmonary fibrosis is classed as WHO Group III, one of the most common groups which lacks effective treatment options. In this study, we aimed to uncover the underlying mechanisms, particularly the involvement of the BMP9/BMPR2/SMAD signalling pathway, in this subtype of pulmonary hypertension.
Experimental Approach
Male Sprague Dawley rats were used to establish a model of pulmonary hypertension with pulmonary fibrosis, induced by bleomycin. Haemodynamic and lung functions were measured, along with histological and immunohistochemical examinations. Primary cultures of rat pulmonary microvascular endothelial cells (PMVECs) were analysed with western blots, apoptosis assays and immunohistochemistry.
Key Results
Early (7 days) after bleomycin treatment of rats, pulmonary arterial thickening and severe loss of pulmonary arterial endothelium were observed, followed (14 days) by increased right ventricular systolic pressure and right ventricular hypertrophy. Marked down‐regulation of the BMP9/BMPR2/SMAD signalling pathway was markedly down‐regulated in lung tissues from bleomycin‐treated rats (throughout the 7‐ to 35‐day treatment period) and bleomycin‐treated rat PMVECs, along with excessive cell apoptosis and loss of pulmonary arterial endothelium. Treatment with recombinant human bone morphogenetic protein 9 (rhBMP9) attenuated these aspects of bleomycin‐induced pulmonary hypertension, by restoring disrupted BMP9/BMPR2/SMAD signalling.
Conclusion and Implications
In bleomycin‐treated rats, early and persisting suppression of the BMP9/BMPR2/SMAD signalling pathway triggered severe loss of pulmonary arterial endothelium and subsequent pulmonary arterial vascular remodelling, contributing to the development of pulmonary hypertension. Therapeutic approaches reinforcing BMP9/BMPR2/SMAD signalling might be ideal strategies for this subtype of pulmonary hypertension.
LINKED ARTICLES
This article is part of a themed issue on Risk factors, comorbidities, and comedications in cardioprotection. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v178.1/issuetoc |
| doi_str_mv | 10.1111/bph.15285 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2452980589</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2471444797</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3885-9c560e6aac0e79ed67ce03f9a2b63f5ca90722da827399f8d08bb17bcc7d25953</originalsourceid><addsrcrecordid>eNp1kU1r3DAQhkVoaTZpD_kDQdBLc3BWki1LOuY7hYSGfpyNJMu7CrLkSjbBPyL_OdpsWkIgc5iBmYd3mHkBOMDoGOdYqmF9jCnhdAcscMXqgpYcfwALhBArMOZ8F-yldI9QHjL6CeyWJeIIVWQBHs_nFM1qcnK0wcPQwdPbO7HM6SdZ_ro9OYfJrrx0zvoVHOS4fpAz1MGP0appNAmOAQ6T64OXcYadVTEkm6D07av2eh5MHI1PmxXWt5M2LVQzVM6EftZ204RRjukz-NhJl8yXl7oP_lxe_D67Lm5-XH0_O7kpdMk5LYSmNTK1lBoZJkxbM21Q2QlJVF12VEuBGCGt5ISVQnS8RVwpzJTWrCVU0HIffNvqDjH8nUwam94mbZyT3oQpNaSiRHBEucjo1zfofZhi_siGYriqKiZYpo62lM7354d2zRBtn29vMGo2HjXZo-bZo8wevihOqjftf_KfKRlYboEH68z8vlJzene9lXwCWSWcwg</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2471444797</pqid></control><display><type>article</type><title>Dysregulation of BMP9/BMPR2/SMAD signalling pathway contributes to pulmonary fibrosis and pulmonary hypertension induced by bleomycin in rats</title><source>Wiley Free Content</source><source>Wiley Online Library Journals Frontfile Complete</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Alma/SFX Local Collection</source><creator>Jiang, Qian ; Liu, Chunli ; Liu, Shiyun ; Lu, Wenju ; Li, Yi ; Luo, Xiaoyun ; Ma, Ran ; Zhang, Chenting ; Chen, Haixia ; Chen, Yuqin ; Zhang, Zizhou ; Hong, Cheng ; Guo, Wenliang ; Wang, Tao ; Yang, Kai ; Wang, Jian</creator><creatorcontrib>Jiang, Qian ; Liu, Chunli ; Liu, Shiyun ; Lu, Wenju ; Li, Yi ; Luo, Xiaoyun ; Ma, Ran ; Zhang, Chenting ; Chen, Haixia ; Chen, Yuqin ; Zhang, Zizhou ; Hong, Cheng ; Guo, Wenliang ; Wang, Tao ; Yang, Kai ; Wang, Jian</creatorcontrib><description>Background and Purpose
Pulmonary hypertension related to pulmonary fibrosis is classed as WHO Group III, one of the most common groups which lacks effective treatment options. In this study, we aimed to uncover the underlying mechanisms, particularly the involvement of the BMP9/BMPR2/SMAD signalling pathway, in this subtype of pulmonary hypertension.
Experimental Approach
Male Sprague Dawley rats were used to establish a model of pulmonary hypertension with pulmonary fibrosis, induced by bleomycin. Haemodynamic and lung functions were measured, along with histological and immunohistochemical examinations. Primary cultures of rat pulmonary microvascular endothelial cells (PMVECs) were analysed with western blots, apoptosis assays and immunohistochemistry.
Key Results
Early (7 days) after bleomycin treatment of rats, pulmonary arterial thickening and severe loss of pulmonary arterial endothelium were observed, followed (14 days) by increased right ventricular systolic pressure and right ventricular hypertrophy. Marked down‐regulation of the BMP9/BMPR2/SMAD signalling pathway was markedly down‐regulated in lung tissues from bleomycin‐treated rats (throughout the 7‐ to 35‐day treatment period) and bleomycin‐treated rat PMVECs, along with excessive cell apoptosis and loss of pulmonary arterial endothelium. Treatment with recombinant human bone morphogenetic protein 9 (rhBMP9) attenuated these aspects of bleomycin‐induced pulmonary hypertension, by restoring disrupted BMP9/BMPR2/SMAD signalling.
Conclusion and Implications
In bleomycin‐treated rats, early and persisting suppression of the BMP9/BMPR2/SMAD signalling pathway triggered severe loss of pulmonary arterial endothelium and subsequent pulmonary arterial vascular remodelling, contributing to the development of pulmonary hypertension. Therapeutic approaches reinforcing BMP9/BMPR2/SMAD signalling might be ideal strategies for this subtype of pulmonary hypertension.
LINKED ARTICLES
This article is part of a themed issue on Risk factors, comorbidities, and comedications in cardioprotection. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v178.1/issuetoc</description><identifier>ISSN: 0007-1188</identifier><identifier>EISSN: 1476-5381</identifier><identifier>DOI: 10.1111/bph.15285</identifier><identifier>PMID: 33080042</identifier><language>eng</language><publisher>England: Blackwell Publishing Ltd</publisher><subject>Apoptosis ; Bleomycin ; Blood pressure ; BMP9 ; BMPR2 ; Bone morphogenetic protein 9 ; Bone morphogenetic protein receptor type II ; endothelial cell ; Endothelial cells ; Endothelium ; Fibrosis ; Heart ; Hypertension ; Hypertrophy ; Immunohistochemistry ; Lung diseases ; Microvasculature ; Pulmonary fibrosis ; Pulmonary hypertension ; Risk factors ; Signal transduction ; Smad protein ; Smad1/5/9 ; Ventricle ; Western blotting</subject><ispartof>British journal of pharmacology, 2021-01, Vol.178 (1), p.203-216</ispartof><rights>2020. The British Pharmacological Society</rights><rights>2020. The British Pharmacological Society.</rights><rights>2021 The British Pharmacological Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3885-9c560e6aac0e79ed67ce03f9a2b63f5ca90722da827399f8d08bb17bcc7d25953</citedby><cites>FETCH-LOGICAL-c3885-9c560e6aac0e79ed67ce03f9a2b63f5ca90722da827399f8d08bb17bcc7d25953</cites><orcidid>0000-0003-3044-2240 ; 0000-0002-1278-256X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fbph.15285$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fbph.15285$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,1427,27901,27902,45550,45551,46384,46808</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33080042$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jiang, Qian</creatorcontrib><creatorcontrib>Liu, Chunli</creatorcontrib><creatorcontrib>Liu, Shiyun</creatorcontrib><creatorcontrib>Lu, Wenju</creatorcontrib><creatorcontrib>Li, Yi</creatorcontrib><creatorcontrib>Luo, Xiaoyun</creatorcontrib><creatorcontrib>Ma, Ran</creatorcontrib><creatorcontrib>Zhang, Chenting</creatorcontrib><creatorcontrib>Chen, Haixia</creatorcontrib><creatorcontrib>Chen, Yuqin</creatorcontrib><creatorcontrib>Zhang, Zizhou</creatorcontrib><creatorcontrib>Hong, Cheng</creatorcontrib><creatorcontrib>Guo, Wenliang</creatorcontrib><creatorcontrib>Wang, Tao</creatorcontrib><creatorcontrib>Yang, Kai</creatorcontrib><creatorcontrib>Wang, Jian</creatorcontrib><title>Dysregulation of BMP9/BMPR2/SMAD signalling pathway contributes to pulmonary fibrosis and pulmonary hypertension induced by bleomycin in rats</title><title>British journal of pharmacology</title><addtitle>Br J Pharmacol</addtitle><description>Background and Purpose
Pulmonary hypertension related to pulmonary fibrosis is classed as WHO Group III, one of the most common groups which lacks effective treatment options. In this study, we aimed to uncover the underlying mechanisms, particularly the involvement of the BMP9/BMPR2/SMAD signalling pathway, in this subtype of pulmonary hypertension.
Experimental Approach
Male Sprague Dawley rats were used to establish a model of pulmonary hypertension with pulmonary fibrosis, induced by bleomycin. Haemodynamic and lung functions were measured, along with histological and immunohistochemical examinations. Primary cultures of rat pulmonary microvascular endothelial cells (PMVECs) were analysed with western blots, apoptosis assays and immunohistochemistry.
Key Results
Early (7 days) after bleomycin treatment of rats, pulmonary arterial thickening and severe loss of pulmonary arterial endothelium were observed, followed (14 days) by increased right ventricular systolic pressure and right ventricular hypertrophy. Marked down‐regulation of the BMP9/BMPR2/SMAD signalling pathway was markedly down‐regulated in lung tissues from bleomycin‐treated rats (throughout the 7‐ to 35‐day treatment period) and bleomycin‐treated rat PMVECs, along with excessive cell apoptosis and loss of pulmonary arterial endothelium. Treatment with recombinant human bone morphogenetic protein 9 (rhBMP9) attenuated these aspects of bleomycin‐induced pulmonary hypertension, by restoring disrupted BMP9/BMPR2/SMAD signalling.
Conclusion and Implications
In bleomycin‐treated rats, early and persisting suppression of the BMP9/BMPR2/SMAD signalling pathway triggered severe loss of pulmonary arterial endothelium and subsequent pulmonary arterial vascular remodelling, contributing to the development of pulmonary hypertension. Therapeutic approaches reinforcing BMP9/BMPR2/SMAD signalling might be ideal strategies for this subtype of pulmonary hypertension.
LINKED ARTICLES
This article is part of a themed issue on Risk factors, comorbidities, and comedications in cardioprotection. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v178.1/issuetoc</description><subject>Apoptosis</subject><subject>Bleomycin</subject><subject>Blood pressure</subject><subject>BMP9</subject><subject>BMPR2</subject><subject>Bone morphogenetic protein 9</subject><subject>Bone morphogenetic protein receptor type II</subject><subject>endothelial cell</subject><subject>Endothelial cells</subject><subject>Endothelium</subject><subject>Fibrosis</subject><subject>Heart</subject><subject>Hypertension</subject><subject>Hypertrophy</subject><subject>Immunohistochemistry</subject><subject>Lung diseases</subject><subject>Microvasculature</subject><subject>Pulmonary fibrosis</subject><subject>Pulmonary hypertension</subject><subject>Risk factors</subject><subject>Signal transduction</subject><subject>Smad protein</subject><subject>Smad1/5/9</subject><subject>Ventricle</subject><subject>Western blotting</subject><issn>0007-1188</issn><issn>1476-5381</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><recordid>eNp1kU1r3DAQhkVoaTZpD_kDQdBLc3BWki1LOuY7hYSGfpyNJMu7CrLkSjbBPyL_OdpsWkIgc5iBmYd3mHkBOMDoGOdYqmF9jCnhdAcscMXqgpYcfwALhBArMOZ8F-yldI9QHjL6CeyWJeIIVWQBHs_nFM1qcnK0wcPQwdPbO7HM6SdZ_ro9OYfJrrx0zvoVHOS4fpAz1MGP0appNAmOAQ6T64OXcYadVTEkm6D07av2eh5MHI1PmxXWt5M2LVQzVM6EftZ204RRjukz-NhJl8yXl7oP_lxe_D67Lm5-XH0_O7kpdMk5LYSmNTK1lBoZJkxbM21Q2QlJVF12VEuBGCGt5ISVQnS8RVwpzJTWrCVU0HIffNvqDjH8nUwam94mbZyT3oQpNaSiRHBEucjo1zfofZhi_siGYriqKiZYpo62lM7354d2zRBtn29vMGo2HjXZo-bZo8wevihOqjftf_KfKRlYboEH68z8vlJzene9lXwCWSWcwg</recordid><startdate>202101</startdate><enddate>202101</enddate><creator>Jiang, Qian</creator><creator>Liu, Chunli</creator><creator>Liu, Shiyun</creator><creator>Lu, Wenju</creator><creator>Li, Yi</creator><creator>Luo, Xiaoyun</creator><creator>Ma, Ran</creator><creator>Zhang, Chenting</creator><creator>Chen, Haixia</creator><creator>Chen, Yuqin</creator><creator>Zhang, Zizhou</creator><creator>Hong, Cheng</creator><creator>Guo, Wenliang</creator><creator>Wang, Tao</creator><creator>Yang, Kai</creator><creator>Wang, Jian</creator><general>Blackwell Publishing Ltd</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7TK</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-3044-2240</orcidid><orcidid>https://orcid.org/0000-0002-1278-256X</orcidid></search><sort><creationdate>202101</creationdate><title>Dysregulation of BMP9/BMPR2/SMAD signalling pathway contributes to pulmonary fibrosis and pulmonary hypertension induced by bleomycin in rats</title><author>Jiang, Qian ; Liu, Chunli ; Liu, Shiyun ; Lu, Wenju ; Li, Yi ; Luo, Xiaoyun ; Ma, Ran ; Zhang, Chenting ; Chen, Haixia ; Chen, Yuqin ; Zhang, Zizhou ; Hong, Cheng ; Guo, Wenliang ; Wang, Tao ; Yang, Kai ; Wang, Jian</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3885-9c560e6aac0e79ed67ce03f9a2b63f5ca90722da827399f8d08bb17bcc7d25953</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Apoptosis</topic><topic>Bleomycin</topic><topic>Blood pressure</topic><topic>BMP9</topic><topic>BMPR2</topic><topic>Bone morphogenetic protein 9</topic><topic>Bone morphogenetic protein receptor type II</topic><topic>endothelial cell</topic><topic>Endothelial cells</topic><topic>Endothelium</topic><topic>Fibrosis</topic><topic>Heart</topic><topic>Hypertension</topic><topic>Hypertrophy</topic><topic>Immunohistochemistry</topic><topic>Lung diseases</topic><topic>Microvasculature</topic><topic>Pulmonary fibrosis</topic><topic>Pulmonary hypertension</topic><topic>Risk factors</topic><topic>Signal transduction</topic><topic>Smad protein</topic><topic>Smad1/5/9</topic><topic>Ventricle</topic><topic>Western blotting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jiang, Qian</creatorcontrib><creatorcontrib>Liu, Chunli</creatorcontrib><creatorcontrib>Liu, Shiyun</creatorcontrib><creatorcontrib>Lu, Wenju</creatorcontrib><creatorcontrib>Li, Yi</creatorcontrib><creatorcontrib>Luo, Xiaoyun</creatorcontrib><creatorcontrib>Ma, Ran</creatorcontrib><creatorcontrib>Zhang, Chenting</creatorcontrib><creatorcontrib>Chen, Haixia</creatorcontrib><creatorcontrib>Chen, Yuqin</creatorcontrib><creatorcontrib>Zhang, Zizhou</creatorcontrib><creatorcontrib>Hong, Cheng</creatorcontrib><creatorcontrib>Guo, Wenliang</creatorcontrib><creatorcontrib>Wang, Tao</creatorcontrib><creatorcontrib>Yang, Kai</creatorcontrib><creatorcontrib>Wang, Jian</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>British journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jiang, Qian</au><au>Liu, Chunli</au><au>Liu, Shiyun</au><au>Lu, Wenju</au><au>Li, Yi</au><au>Luo, Xiaoyun</au><au>Ma, Ran</au><au>Zhang, Chenting</au><au>Chen, Haixia</au><au>Chen, Yuqin</au><au>Zhang, Zizhou</au><au>Hong, Cheng</au><au>Guo, Wenliang</au><au>Wang, Tao</au><au>Yang, Kai</au><au>Wang, Jian</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Dysregulation of BMP9/BMPR2/SMAD signalling pathway contributes to pulmonary fibrosis and pulmonary hypertension induced by bleomycin in rats</atitle><jtitle>British journal of pharmacology</jtitle><addtitle>Br J Pharmacol</addtitle><date>2021-01</date><risdate>2021</risdate><volume>178</volume><issue>1</issue><spage>203</spage><epage>216</epage><pages>203-216</pages><issn>0007-1188</issn><eissn>1476-5381</eissn><abstract>Background and Purpose
Pulmonary hypertension related to pulmonary fibrosis is classed as WHO Group III, one of the most common groups which lacks effective treatment options. In this study, we aimed to uncover the underlying mechanisms, particularly the involvement of the BMP9/BMPR2/SMAD signalling pathway, in this subtype of pulmonary hypertension.
Experimental Approach
Male Sprague Dawley rats were used to establish a model of pulmonary hypertension with pulmonary fibrosis, induced by bleomycin. Haemodynamic and lung functions were measured, along with histological and immunohistochemical examinations. Primary cultures of rat pulmonary microvascular endothelial cells (PMVECs) were analysed with western blots, apoptosis assays and immunohistochemistry.
Key Results
Early (7 days) after bleomycin treatment of rats, pulmonary arterial thickening and severe loss of pulmonary arterial endothelium were observed, followed (14 days) by increased right ventricular systolic pressure and right ventricular hypertrophy. Marked down‐regulation of the BMP9/BMPR2/SMAD signalling pathway was markedly down‐regulated in lung tissues from bleomycin‐treated rats (throughout the 7‐ to 35‐day treatment period) and bleomycin‐treated rat PMVECs, along with excessive cell apoptosis and loss of pulmonary arterial endothelium. Treatment with recombinant human bone morphogenetic protein 9 (rhBMP9) attenuated these aspects of bleomycin‐induced pulmonary hypertension, by restoring disrupted BMP9/BMPR2/SMAD signalling.
Conclusion and Implications
In bleomycin‐treated rats, early and persisting suppression of the BMP9/BMPR2/SMAD signalling pathway triggered severe loss of pulmonary arterial endothelium and subsequent pulmonary arterial vascular remodelling, contributing to the development of pulmonary hypertension. Therapeutic approaches reinforcing BMP9/BMPR2/SMAD signalling might be ideal strategies for this subtype of pulmonary hypertension.
LINKED ARTICLES
This article is part of a themed issue on Risk factors, comorbidities, and comedications in cardioprotection. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v178.1/issuetoc</abstract><cop>England</cop><pub>Blackwell Publishing Ltd</pub><pmid>33080042</pmid><doi>10.1111/bph.15285</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0003-3044-2240</orcidid><orcidid>https://orcid.org/0000-0002-1278-256X</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Apoptosis Bleomycin Blood pressure BMP9 BMPR2 Bone morphogenetic protein 9 Bone morphogenetic protein receptor type II endothelial cell Endothelial cells Endothelium Fibrosis Heart Hypertension Hypertrophy Immunohistochemistry Lung diseases Microvasculature Pulmonary fibrosis Pulmonary hypertension Risk factors Signal transduction Smad protein Smad1/5/9 Ventricle Western blotting |
| title | Dysregulation of BMP9/BMPR2/SMAD signalling pathway contributes to pulmonary fibrosis and pulmonary hypertension induced by bleomycin in rats |
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