| Model . | Organ specificity . | Cardiovascular stress . | Cardiovascular phenotype . | Ref . |
|---|---|---|---|---|
| PARP1 deficiency | Systemic | HFD and ApoE−/− | Reduced atherosclerotic plaque formation and size | 69–72 |
| I/R | Attenuated myocardial injury, disrupted myocardial structure, mitochondrial dysfunction, MMP, and neutrophil infiltration | 73,74 | ||
| Hyperglycemia | Reduced diabetic arteriosclerotic calcification, regulated synthetic phenotype switching of VSMC | 75 | ||
| Ang II-induced cardiac hypertrophy | Attenuated cardiac hypertrophy and interstitial fibrosis | 76 | ||
| Ang II-induced AAA | Decreased AAA incidence, abdominal aortic diameter, and macrophage infiltration | 77 | ||
| PARP2 deficiency | Systemic | Doxorubicin | Decreased vascular damage and mitochondrial dysfunction | 78 |
| ATM deficiency | Systemic | TAC | Attenuated LV dysfunction, improved mortality, and alleviated NF-κB-mediated inflammation | 29 |
| MI | Attenuated LV dysfunction, dilation and inflammation in early post-MI (1–7 days), exacerbated LV dysfunction, fibrosis, apoptosis, and cardiac hypertrophy in late post-MI (14–28 days) | 79–83 | ||
| ApoE−/− | Accelerated atherosclerosis and multiple features of metabolic syndrome | 84,85 | ||
| Hyperglycemia | Attenuated endothelial dysfunction and senescence induced by injection of STZ | 48 | ||
| Cardiomyocyte-specific | TAC | Attenuated cardiac hypertrophy | 21 | |
| Cardiac fibroblast-specific | Doxorubicin | Attenuated LV dysfunction, cardiac apoptosis and mortality | 52 | |
| DNA-PKcs deficiency | Cardiac | I/R | Reserved cardiac function, reduced myocardial injury, attenuated apoptosis and inflammation | 86 |
| p53 deficiency | Cardiac | TAC | Attenuated cardiac hypertrophy, injury, and dysfunction | 87 |
| Systemic | MI | Reduced incidence of LV rupture post-MI | 88 | |
| BRCA1 deficiency | Cardiomyocyte-specific | MI | Increased mortality, exaggerated LV dilation, increased apoptosis, and impaired DSB repair | 9 |
| NBS1 overexpression | VSMC-specific | HFD and ApoE−/− | Enhanced DSB repair, decreased apoptosis and growth arrest, increased fibrous cap area and plaque stability | 23 |
| OGG1 deficiency | Systemic | Western diet and Ldlr−/− | Increased plaque size and lipid content, DNA damage, apoptosis, and inflammation | 31 |
| Model . | Organ specificity . | Cardiovascular stress . | Cardiovascular phenotype . | Ref . |
|---|---|---|---|---|
| PARP1 deficiency | Systemic | HFD and ApoE−/− | Reduced atherosclerotic plaque formation and size | 69–72 |
| I/R | Attenuated myocardial injury, disrupted myocardial structure, mitochondrial dysfunction, MMP, and neutrophil infiltration | 73,74 | ||
| Hyperglycemia | Reduced diabetic arteriosclerotic calcification, regulated synthetic phenotype switching of VSMC | 75 | ||
| Ang II-induced cardiac hypertrophy | Attenuated cardiac hypertrophy and interstitial fibrosis | 76 | ||
| Ang II-induced AAA | Decreased AAA incidence, abdominal aortic diameter, and macrophage infiltration | 77 | ||
| PARP2 deficiency | Systemic | Doxorubicin | Decreased vascular damage and mitochondrial dysfunction | 78 |
| ATM deficiency | Systemic | TAC | Attenuated LV dysfunction, improved mortality, and alleviated NF-κB-mediated inflammation | 29 |
| MI | Attenuated LV dysfunction, dilation and inflammation in early post-MI (1–7 days), exacerbated LV dysfunction, fibrosis, apoptosis, and cardiac hypertrophy in late post-MI (14–28 days) | 79–83 | ||
| ApoE−/− | Accelerated atherosclerosis and multiple features of metabolic syndrome | 84,85 | ||
| Hyperglycemia | Attenuated endothelial dysfunction and senescence induced by injection of STZ | 48 | ||
| Cardiomyocyte-specific | TAC | Attenuated cardiac hypertrophy | 21 | |
| Cardiac fibroblast-specific | Doxorubicin | Attenuated LV dysfunction, cardiac apoptosis and mortality | 52 | |
| DNA-PKcs deficiency | Cardiac | I/R | Reserved cardiac function, reduced myocardial injury, attenuated apoptosis and inflammation | 86 |
| p53 deficiency | Cardiac | TAC | Attenuated cardiac hypertrophy, injury, and dysfunction | 87 |
| Systemic | MI | Reduced incidence of LV rupture post-MI | 88 | |
| BRCA1 deficiency | Cardiomyocyte-specific | MI | Increased mortality, exaggerated LV dilation, increased apoptosis, and impaired DSB repair | 9 |
| NBS1 overexpression | VSMC-specific | HFD and ApoE−/− | Enhanced DSB repair, decreased apoptosis and growth arrest, increased fibrous cap area and plaque stability | 23 |
| OGG1 deficiency | Systemic | Western diet and Ldlr−/− | Increased plaque size and lipid content, DNA damage, apoptosis, and inflammation | 31 |
AAA, abdominal aortic aneurysm; HFD, high-fat diet; STZ, streptozotocin; TAC, transverse aortic constriction.
| Model . | Organ specificity . | Cardiovascular stress . | Cardiovascular phenotype . | Ref . |
|---|---|---|---|---|
| PARP1 deficiency | Systemic | HFD and ApoE−/− | Reduced atherosclerotic plaque formation and size | 69–72 |
| I/R | Attenuated myocardial injury, disrupted myocardial structure, mitochondrial dysfunction, MMP, and neutrophil infiltration | 73,74 | ||
| Hyperglycemia | Reduced diabetic arteriosclerotic calcification, regulated synthetic phenotype switching of VSMC | 75 | ||
| Ang II-induced cardiac hypertrophy | Attenuated cardiac hypertrophy and interstitial fibrosis | 76 | ||
| Ang II-induced AAA | Decreased AAA incidence, abdominal aortic diameter, and macrophage infiltration | 77 | ||
| PARP2 deficiency | Systemic | Doxorubicin | Decreased vascular damage and mitochondrial dysfunction | 78 |
| ATM deficiency | Systemic | TAC | Attenuated LV dysfunction, improved mortality, and alleviated NF-κB-mediated inflammation | 29 |
| MI | Attenuated LV dysfunction, dilation and inflammation in early post-MI (1–7 days), exacerbated LV dysfunction, fibrosis, apoptosis, and cardiac hypertrophy in late post-MI (14–28 days) | 79–83 | ||
| ApoE−/− | Accelerated atherosclerosis and multiple features of metabolic syndrome | 84,85 | ||
| Hyperglycemia | Attenuated endothelial dysfunction and senescence induced by injection of STZ | 48 | ||
| Cardiomyocyte-specific | TAC | Attenuated cardiac hypertrophy | 21 | |
| Cardiac fibroblast-specific | Doxorubicin | Attenuated LV dysfunction, cardiac apoptosis and mortality | 52 | |
| DNA-PKcs deficiency | Cardiac | I/R | Reserved cardiac function, reduced myocardial injury, attenuated apoptosis and inflammation | 86 |
| p53 deficiency | Cardiac | TAC | Attenuated cardiac hypertrophy, injury, and dysfunction | 87 |
| Systemic | MI | Reduced incidence of LV rupture post-MI | 88 | |
| BRCA1 deficiency | Cardiomyocyte-specific | MI | Increased mortality, exaggerated LV dilation, increased apoptosis, and impaired DSB repair | 9 |
| NBS1 overexpression | VSMC-specific | HFD and ApoE−/− | Enhanced DSB repair, decreased apoptosis and growth arrest, increased fibrous cap area and plaque stability | 23 |
| OGG1 deficiency | Systemic | Western diet and Ldlr−/− | Increased plaque size and lipid content, DNA damage, apoptosis, and inflammation | 31 |
| Model . | Organ specificity . | Cardiovascular stress . | Cardiovascular phenotype . | Ref . |
|---|---|---|---|---|
| PARP1 deficiency | Systemic | HFD and ApoE−/− | Reduced atherosclerotic plaque formation and size | 69–72 |
| I/R | Attenuated myocardial injury, disrupted myocardial structure, mitochondrial dysfunction, MMP, and neutrophil infiltration | 73,74 | ||
| Hyperglycemia | Reduced diabetic arteriosclerotic calcification, regulated synthetic phenotype switching of VSMC | 75 | ||
| Ang II-induced cardiac hypertrophy | Attenuated cardiac hypertrophy and interstitial fibrosis | 76 | ||
| Ang II-induced AAA | Decreased AAA incidence, abdominal aortic diameter, and macrophage infiltration | 77 | ||
| PARP2 deficiency | Systemic | Doxorubicin | Decreased vascular damage and mitochondrial dysfunction | 78 |
| ATM deficiency | Systemic | TAC | Attenuated LV dysfunction, improved mortality, and alleviated NF-κB-mediated inflammation | 29 |
| MI | Attenuated LV dysfunction, dilation and inflammation in early post-MI (1–7 days), exacerbated LV dysfunction, fibrosis, apoptosis, and cardiac hypertrophy in late post-MI (14–28 days) | 79–83 | ||
| ApoE−/− | Accelerated atherosclerosis and multiple features of metabolic syndrome | 84,85 | ||
| Hyperglycemia | Attenuated endothelial dysfunction and senescence induced by injection of STZ | 48 | ||
| Cardiomyocyte-specific | TAC | Attenuated cardiac hypertrophy | 21 | |
| Cardiac fibroblast-specific | Doxorubicin | Attenuated LV dysfunction, cardiac apoptosis and mortality | 52 | |
| DNA-PKcs deficiency | Cardiac | I/R | Reserved cardiac function, reduced myocardial injury, attenuated apoptosis and inflammation | 86 |
| p53 deficiency | Cardiac | TAC | Attenuated cardiac hypertrophy, injury, and dysfunction | 87 |
| Systemic | MI | Reduced incidence of LV rupture post-MI | 88 | |
| BRCA1 deficiency | Cardiomyocyte-specific | MI | Increased mortality, exaggerated LV dilation, increased apoptosis, and impaired DSB repair | 9 |
| NBS1 overexpression | VSMC-specific | HFD and ApoE−/− | Enhanced DSB repair, decreased apoptosis and growth arrest, increased fibrous cap area and plaque stability | 23 |
| OGG1 deficiency | Systemic | Western diet and Ldlr−/− | Increased plaque size and lipid content, DNA damage, apoptosis, and inflammation | 31 |
AAA, abdominal aortic aneurysm; HFD, high-fat diet; STZ, streptozotocin; TAC, transverse aortic constriction.
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