Activation of hypoxia-sensing pathways promotes renal ischemic preconditioning following myocardial infarction
| العنوان: | Activation of hypoxia-sensing pathways promotes renal ischemic preconditioning following myocardial infarction |
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| المؤلفون: | Andrew S. Terker, Sochinweichi Nwosisi, Suwan Wang, Xiaofeng Fan, Aolei Niu, Yahua Zhang, Raymond C. Harris, Kensuke Sasaki, Ming-Zhi Zhang, Juan Pablo Arroyo |
| المصدر: | Am J Physiol Renal Physiol |
| بيانات النشر: | American Physiological Society, 2021. |
| سنة النشر: | 2021 |
| مصطلحات موضوعية: | medicine.medical_specialty, Physiology, Myocardial Infarction, Cardiorenal syndrome, Kidney, Internal medicine, medicine, Kidney injury, Animals, Myocardial infarction, Renal Insufficiency, Chronic, Hypoxia, Ischemic Preconditioning, Heart Failure, Cardio-Renal Syndrome, business.industry, Myocardium, Acute kidney injury, Heart, Acute Kidney Injury, Hypoxia (medical), medicine.disease, Hypoxia-inducible factors, Cardiology, Ischemic preconditioning, medicine.symptom, business, Research Article |
| الوصف: | Ischemic heart disease is the leading cause of death worldwide and is frequently comorbid with chronic kidney disease. Physiological communication is known to occur between the heart and the kidney. Although primary dysfunction in either organ can induce dysfunction in the other, a clinical entity known as cardiorenal syndrome, mechanistic details are lacking. Here, we used a model of experimental myocardial infarction (MI) to test effects of chronic cardiac ischemia on acute and chronic kidney injury. Surprisingly, chronic cardiac damage protected animals from subsequent acute ischemic renal injury, an effect that was accompanied by evidence of chronic kidney hypoxia. The protection observed post-MI was similar to protection observed in a separate group of healthy animals housed in ambient hypoxic conditions prior to kidney injury, suggesting a common mechanism. There was evidence that chronic cardiac injury activates renal hypoxia-sensing pathways. Increased renal abundance of several glycolytic enzymes following MI suggested that a shift toward glycolysis may confer renal ischemic preconditioning. In contrast, effects on chronic renal injury followed a different pattern, with post-MI animals displaying worsened chronic renal injury and fibrosis. These data show that although chronic cardiac injury following MI protected against acute kidney injury via activation of hypoxia-sensing pathways, it worsened chronic kidney injury. The results further our understanding of cardiorenal signaling mechanisms and have implications for the treatment of heart failure patients with associated renal disease. NEW & NOTEWORTHY Experimental myocardial infarction (MI) protects from subsequent ischemic acute kidney injury but worsens chronic kidney injury. Observed protection from ischemic acute kidney injury after MI was accompanied by chronic kidney hypoxia and increased renal abundance of hypoxia-inducible transcripts. These data support the idea that MI confers protection from renal ischemic injury via chronic renal hypoxia and activation of downstream hypoxia-inducible signaling pathways. |
| تدمد: | 1522-1466 1931-857X |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::254cee55c02c86ae7beb47835f70cdb2Test https://doi.org/10.1152/ajprenal.00476.2020Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....254cee55c02c86ae7beb47835f70cdb2 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 15221466 1931857X |
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