Mouse models for abdominal aortic aneurysm

Abdominal aortic aneurysm (AAA) rupture is estimated to cause 200,000 deaths each year. Currently, the only treatment for AAA is surgical repair; however, this is only indicated for large asymptomatic, symptomatic or ruptured aneurysms, is not always durable, and is associated with a risk of serious...

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Published inBritish journal of pharmacology Vol. 179; no. 5; pp. 792 - 810
Main Authors Golledge, Jonathan, Krishna, Smriti Murali, Wang, Yutang
Format Journal Article
LanguageEnglish
Published England Blackwell Publishing Ltd 01.03.2022
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Abstract Abdominal aortic aneurysm (AAA) rupture is estimated to cause 200,000 deaths each year. Currently, the only treatment for AAA is surgical repair; however, this is only indicated for large asymptomatic, symptomatic or ruptured aneurysms, is not always durable, and is associated with a risk of serious perioperative complications. As a result, patients with small asymptomatic aneurysms or who are otherwise unfit for surgery are treated conservatively, but up to 70% of small aneurysms continue to grow, increasing the risk of rupture. There is thus an urgent need to develop drug therapies effective at slowing AAA growth. This review describes the commonly used mouse models for AAA. Recent research in these models highlights key roles for pathways involved in inflammation and cell turnover in AAA pathogenesis. There is also evidence for long non‐coding RNAs and thrombosis in aneurysm pathology. Further well‐designed research in clinically relevant models is expected to be translated into effective AAA drugs. LINKED ARTICLES This article is part of a themed issue on Preclinical Models for Cardiovascular disease research (BJP 75th Anniversary). To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v179.5/issuetoc Innate and adaptive immunity, autophagy, protease‐mediated extracellular matrix remodelling, hydroxyapatite‐mediated microcalcification, epigenetic changes, and intraluminal thrombus are strongly implicated in abdominal aortic aneurysm (AAA). Immune response regulators, autophagy promoting agents, protease inhibitors, siRNA inhibiting hydroxyapatite formation, microRNAs, and coagulation cascade inhibitors have been reported to limit AAA development in mice.
AbstractList Abdominal aortic aneurysm (AAA) rupture is estimated to cause 200,000 deaths each year. Currently, the only treatment for AAA is surgical repair; however, this is only indicated for large asymptomatic, symptomatic or ruptured aneurysms, is not always durable, and is associated with a risk of serious perioperative complications. As a result, patients with small asymptomatic aneurysms or who are otherwise unfit for surgery are treated conservatively, but up to 70% of small aneurysms continue to grow, increasing the risk of rupture. There is thus an urgent need to develop drug therapies effective at slowing AAA growth. This review describes the commonly used mouse models for AAA. Recent research in these models highlights key roles for pathways involved in inflammation and cell turnover in AAA pathogenesis. There is also evidence for long non‐coding RNAs and thrombosis in aneurysm pathology. Further well‐designed research in clinically relevant models is expected to be translated into effective AAA drugs.LINKED ARTICLESThis article is part of a themed issue on Preclinical Models for Cardiovascular disease research (BJP 75th Anniversary). To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v179.5/issuetoc
Abdominal aortic aneurysm (AAA) rupture is estimated to cause 200,000 deaths each year. Currently, the only treatment for AAA is surgical repair; however, this is only indicated for large asymptomatic, symptomatic or ruptured aneurysms, is not always durable, and is associated with a risk of serious perioperative complications. As a result, patients with small asymptomatic aneurysms or who are otherwise unfit for surgery are treated conservatively, but up to 70% of small aneurysms continue to grow, increasing the risk of rupture. There is thus an urgent need to develop drug therapies effective at slowing AAA growth. This review describes the commonly used mouse models for AAA. Recent research in these models highlights key roles for pathways involved in inflammation and cell turnover in AAA pathogenesis. There is also evidence for long non-coding RNAs and thrombosis in aneurysm pathology. Further well-designed research in clinically relevant models is expected to be translated into effective AAA drugs. LINKED ARTICLES: This article is part of a themed issue on Preclinical Models for Cardiovascular disease research (BJP 75th Anniversary). To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v179.5/issuetoc.Abdominal aortic aneurysm (AAA) rupture is estimated to cause 200,000 deaths each year. Currently, the only treatment for AAA is surgical repair; however, this is only indicated for large asymptomatic, symptomatic or ruptured aneurysms, is not always durable, and is associated with a risk of serious perioperative complications. As a result, patients with small asymptomatic aneurysms or who are otherwise unfit for surgery are treated conservatively, but up to 70% of small aneurysms continue to grow, increasing the risk of rupture. There is thus an urgent need to develop drug therapies effective at slowing AAA growth. This review describes the commonly used mouse models for AAA. Recent research in these models highlights key roles for pathways involved in inflammation and cell turnover in AAA pathogenesis. There is also evidence for long non-coding RNAs and thrombosis in aneurysm pathology. Further well-designed research in clinically relevant models is expected to be translated into effective AAA drugs. LINKED ARTICLES: This article is part of a themed issue on Preclinical Models for Cardiovascular disease research (BJP 75th Anniversary). To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v179.5/issuetoc.
Abdominal aortic aneurysm (AAA) rupture is estimated to cause 200,000 deaths each year. Currently, the only treatment for AAA is surgical repair; however, this is only indicated for large asymptomatic, symptomatic or ruptured aneurysms, is not always durable, and is associated with a risk of serious perioperative complications. As a result, patients with small asymptomatic aneurysms or who are otherwise unfit for surgery are treated conservatively, but up to 70% of small aneurysms continue to grow, increasing the risk of rupture. There is thus an urgent need to develop drug therapies effective at slowing AAA growth. This review describes the commonly used mouse models for AAA. Recent research in these models highlights key roles for pathways involved in inflammation and cell turnover in AAA pathogenesis. There is also evidence for long non-coding RNAs and thrombosis in aneurysm pathology. Further well-designed research in clinically relevant models is expected to be translated into effective AAA drugs. LINKED ARTICLES: This article is part of a themed issue on Preclinical Models for Cardiovascular disease research (BJP 75th Anniversary). To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v179.5/issuetoc.
Abdominal aortic aneurysm (AAA) rupture is estimated to cause 200,000 deaths each year. Currently, the only treatment for AAA is surgical repair; however, this is only indicated for large asymptomatic, symptomatic or ruptured aneurysms, is not always durable, and is associated with a risk of serious perioperative complications. As a result, patients with small asymptomatic aneurysms or who are otherwise unfit for surgery are treated conservatively, but up to 70% of small aneurysms continue to grow, increasing the risk of rupture. There is thus an urgent need to develop drug therapies effective at slowing AAA growth. This review describes the commonly used mouse models for AAA. Recent research in these models highlights key roles for pathways involved in inflammation and cell turnover in AAA pathogenesis. There is also evidence for long non‐coding RNAs and thrombosis in aneurysm pathology. Further well‐designed research in clinically relevant models is expected to be translated into effective AAA drugs. LINKED ARTICLES This article is part of a themed issue on Preclinical Models for Cardiovascular disease research (BJP 75th Anniversary). To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v179.5/issuetoc Innate and adaptive immunity, autophagy, protease‐mediated extracellular matrix remodelling, hydroxyapatite‐mediated microcalcification, epigenetic changes, and intraluminal thrombus are strongly implicated in abdominal aortic aneurysm (AAA). Immune response regulators, autophagy promoting agents, protease inhibitors, siRNA inhibiting hydroxyapatite formation, microRNAs, and coagulation cascade inhibitors have been reported to limit AAA development in mice.
Author Krishna, Smriti Murali
Golledge, Jonathan
Wang, Yutang
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2004; 24
2011; 53
2019; 16
2020; 15
2019; 19
2019; 289
2019; 322
2019; 202
2020; 13
2020; 288
2020; 323
2020; 10
2008; 102
2009; 119
2016; 37
2016; 36
2018; 7
2001; 134
2018; 39
2009; 10
2019; 24
2019; 23
2006; 26
2015; 373
2008; 117
2020; 177
2019; 317
2002; 90
2014a; 9
2009; 16
2018; 38
2019; 9
2020; 40
2020; 142
2020; 143
2017; 66
2013; 226
2005; 115
2017; 65
1997; 25
2019; 34
2019a; 176
2012; 181
2019; 39
2019; 38
2013; 100
2016; 18
2016; 281
2019; 460
2017; 135
2019; 42
2019; 41
2000; 105
2018; 118
2015; 65
2015; 2015
2020; 26
2017; 261
2019; 856
2019; 217
2001; 34
1999; 878
2019; 176
2003; 23
2015; 35
2010; 55
2013; 22
2015; 105
2015; 102
2020; 60
2019; 57
2020; 57
1999; 126
2017; 113
2014b; 9
2020; 6
2017; 37
2020; 251
2016; 119
2013; 159
2020; 9
2019; 115
2002; 106
2019; 116
2019; 234
2002; 346
2020; 134
2009; 284
2018; 71
2007; 20
2019b; 176
2007; 27
2015; 6
2015; 16
2019; 73
2011; 217
2008; 18
2002; 35
2011; 31
2016; 53
2017; 170
2016; 52
2011; 32
2010; 120
2006; 1
2018; 67
2009; 26
2014; 233
2017; 14
2020
2020; 72
2015; 22
2002; 287
2015; 21
2011; 41
2019
2020; 116
2015
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2019; 130
2012; 7
2019; 133
2019; 132
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Snippet Abdominal aortic aneurysm (AAA) rupture is estimated to cause 200,000 deaths each year. Currently, the only treatment for AAA is surgical repair; however, this...
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SubjectTerms abdominal aortic aneurysm
Animal models
Animals
Aortic Aneurysm, Abdominal - drug therapy
Aortic aneurysms
Aortic Rupture - complications
Aortic Rupture - surgery
Asymptomatic
Cardiovascular diseases
Disease Models, Animal
Humans
Mice
mouse models
pathology
Rupture
Thrombosis
Title Mouse models for abdominal aortic aneurysm
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fbph.15260
https://www.ncbi.nlm.nih.gov/pubmed/32914434
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