scholarly journals Myocardial Injury Promotes Matrix Metalloproteinase-9 Activity in the Renal Cortex in Preclinical Models of Acute Myocardial Infarction

Author(s):  
Xiaoying Qiao ◽  
Shreyas Bhave ◽  
Lija Swain ◽  
Elric Zweck ◽  
Lara Reyelt ◽  
...  

AbstractNew mechanistic insight into how the kidney responds to cardiac injury during acute myocardial infarction (AMI) is required. We hypothesized that AMI promotes inflammation and matrix metalloproteinase-9 (MMP9) activity in the kidney and studied the effect of initiating an Impella CP or veno-arterial extracorporeal membrane oxygenation (VA-ECMO) before coronary reperfusion during AMI. Adult male swine were subjected to coronary occlusion and either reperfusion (ischemia-reperfusion; IR) or support with either Impella or VA-ECMO before reperfusion. IR and ECMO increased while Impella reduced levels of MMP-9 in the myocardial infarct zone, circulation, and renal cortex. Compared to IR, Impella reduced myocardial infarct size and urinary KIM-1 levels, but VA-ECMO did not. IR and VA-ECMO increased pro-fibrogenic signaling via transforming growth factor-beta and endoglin in the renal cortex, but Impella did not. These findings identify that AMI increases inflammatory activity in the kidney, which may be attenuated by Impella support.

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Lichan Tao ◽  
Yihua Bei ◽  
Haifeng Zhang ◽  
Yanli Zhou ◽  
Jingfa Jiang ◽  
...  

Acute myocardial infarction (AMI) represents a major cause of morbidity and mortality worldwide. Exercise has been proved to reduce myocardial ischemia-reperfusion (I/R) injury. However it remains unclear whether, and (if so) how, exercise could protect against AMI. Methods: Mice were trained using a 3-week swimming protocol, and then subjected to left coronary artery (LCA) ligation, and finally sacrificed 24 h after AMI. Results: Exercise training reduces myocardial infarct size and abolishes AMI-induced autophagy and apoptosis. MI leads to a shift from fatty acid to glucose metabolism in the myocardium with a downregulation of PPAR-α and PPAR-γ. Also, AMI induces an adaptive increase of mitochondrial DNA replication and transcription in the acute phase of MI, accompanied by an activation of PGC-1α signaling. Exercise abolishes the derangement of myocardial glucose and lipid metabolism and further enhances the adaptive increase of mitochondrial biogenesis. Conclusion: Exercise training protects against AMI-induced acute cardiac injury through improving myocardial energy metabolism and enhancing the early adaptive change of mitochondrial biogenesis.


2009 ◽  
Vol 42 (4-5) ◽  
pp. 342
Author(s):  
Savas Guzel ◽  
Ozden Serin ◽  
Guzin Yilmaz ◽  
Eda Celik Guzel ◽  
Guvenc Guvenen

2004 ◽  
Vol 68 (5) ◽  
pp. 451-454 ◽  
Author(s):  
Hiroshi Funayama ◽  
San-e Ishikawa ◽  
Norifumi Kubo ◽  
Takuji Katayama ◽  
Takanori Yasu ◽  
...  

2006 ◽  
Vol 12 (1) ◽  
pp. 66-72 ◽  
Author(s):  
Daniel R. Wagner ◽  
Charles Delagardelle ◽  
Isabelle Ernens ◽  
Didier Rouy ◽  
Michel Vaillant ◽  
...  

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