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Abstract
Objective Understanding the multifactorial changes involved in the kidney and heart after acute myocardial infarction (AMI) is prerequisite for further mechanisms and early intervention, especially autophagy changes. Here, we discussed the role of adaptive autophagy in the heart and kidney of rats with AMI. Methods A rat model of AMI was established by ligating the left anterior descending branch of the coronary artery. Animals were sacrificed at 2 and 4 weeks after the operation to assess the morphological and functional changes of the heart and kidney, as well as the autophagy pathway. In vitro, HK-2 and AC16 cell injuries and the autophagy pathway were assayed after autophagy was inhibited by 3-methyladenine (3-MA) in a hypoxia incubator. Results We found that the left ventricular systolic pressure (LVSP) significantly decreased in the model group at weeks 2 and 4. At weeks 2 and 4, the level of urinary kidney injury molecule 1 (uKIM1) of the model group was significantly higher than the sham group. At week 4, urinary neutrophil gelatinase-associated lipocalcin (uNGAL) and urinary albumin also significantly increased. At week 2, microtubule-associated protein 1 light chain 3-II (LC3-II), ATG5, and Beclin1 were significantly elevated in the heart and kidney compared with the sham-operated rats, but there was no change in p62 levels. At week 4, LC3-II did not significantly increase and p62 levels significantly increased. In addition, 3-MA markedly increased KIM1, NGAL, and the activity of caspase-3 in the hypoxic HK-2 and AC16 cell. Conclusion Autophagy will undergo adaptive changes and play a protective role in the heart and kidney of rats after AMI.
Highlights
At present, acute myocardial infarction (AMI) accounts for the highest proportion of coronary heart disease in China [1]
We found that the renal tubular injury marker urinary kidney injury molecule 1 (uKIM1) in the model group was significantly higher than the sham group at week 2, but there was no increase in the level of urinary neutrophil gelatinase-associated lipocalcin (uNGAL)
Our TUNEL results indicated that apoptotic myocardial cells were significantly increased in the model group at weeks 2 and 4, and the rate of apoptosis in renal tubular cells significantly increased at week 4, but did not increase at week 2 (Figure 1(b))
Summary
AMI accounts for the highest proportion of coronary heart disease in China [1]. It plays a crucial role in the pathogenesis of the kidney and heart diseases [7]. Few studies have observed autophagy changes in the heart and kidney at the same time and whether their changes are consistent. This is the basis of the use of autophagy in treating cardiorenal syndrome. Considering these facts, in our study, we tested the role of autophagy in the heart and kidney of rats after acute myocardial infarction (AMI). We clarify whether the changes are consistent in the heart and kidney, and elucidate the protective effect of adaptive autophagy
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