Kalbin Enerji Metabolizması: Kalp Yetmezliğinde ve Kardiyomiyopatide Enerji Metabolizmasında Görülen Değişikler

Year 2025, Volume: 1 Issue: 3, 1 - 8, 15.06.2025

Osman Kağan Çakır , Renad Mammadov , Hatice Cakir

Abstract

Kalp, enerji ihtiyacı çok yüksek olan bir organdır ve kasılma fonksiyonunu devam ettirebilmek için devamlı ATP üretmesi gerekir. Kalp, kasılma görevinin devamlılığı için gerekli olan ATP'yi iki ana kaynaktan sağlar. Bunlar; mitokondriyal oksidatif fosforilasyon ve glikolizdir. Mitokondriyal oksidatif fosforilasyon miyokardiyal ATP ihtiyacının büyük bir kısmını sağlar. Sağlıklı kalp metabolik olarak çeşitli enerji kaynaklarını kullanabilir, metabolik olarak esnektir. ATP üretiminde en büyük katkı sağlayan substrat yağ asitleridir, ardından laktat, keton cisimleri, glukoz ve daha sonra dallı zincirli amino asitler katkı sağlar. ATP üretilmesindeki düzensizliğin kardiyak performans üzerinde önemli etkileri bulunmaktadır. Yayınlanmış literatürler PubMed, SciFinder, ScienceDirect, Wiley Online Library, Google Scholar ve Web of Science gibi bilimsel veri tabanlarından Aralık 2024'e kadar toplanmıştır. Bu derlemede, kalpteki ATP üretilmesine ilişkin mevcut bilgiler, enerji metabolizmasına bağlı görülebilecek durumlar ile ilgili güncel perspektifler tartışılacaktır.

Keywords

Kalp , ATP , Kalp Yetmezliği , Kardiyomiyopati , Kalbin Enerji Metabolizması

References

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• Tong, M., Zablocki, D., & Sadoshima, J. (2020). The role of Drp1 in mitophagy and cell death in the heart. Journal of Molecular and Cellular Cardiology, 142, 138-145.
• Vakrou, S., & Abraham, M. R. (2014). Hypertrophic cardiomyopathy: a heart in need of an energy bar? Frontiers in Physiology, 5, 309.
• Yamada, S., Kane, G. C., Behfar, A., Liu, X. K., Dyer, R. B., Faustino, R. S., Miki, T., Seino, S., & Terzic, A. (2006). Protection conferred by myocardial ATP‐sensitive K+ channels in pressure overload‐induced congestive heart failure revealed in KCNJ11 Kir6. 2‐null mutant. The Journal of Physiology, 577(3), 1053-1065.
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• Bienengraeber, M., Olson, T. M., Selivanov, V. A., Kathmann, E. C., O'Cochlain, F., Gao, F., & Zingman, L. V. (2004). ABCC9 mutations identified in human dilated cardiomyopathy disrupt catalytic KATP channel gating. Nature Genetics, 36(4), 382-387.
• Bornstein, M. R., Tian, R., & Arany, Z. (2024). Human cardiac metabolism. Cell Metabolism, 36(7), 1456-1481. Bottomley, P. A., Panjrath, G. S., Lai, S., Hirsch, G. A., Wu, K., Najjar, S. S., Steinberg, A. S., Gerstenblith, G., & Weiss, R. (2013). Metabolic rates of ATP transfer through creatine kinase (CK Flux) predict clinical heart failure events and death. Science Translational Medicine, 5(215), 215re3-215re3.
• Hensley, N., Dietrich, J., Nyhan, D., Mitter, N., Yee, M. S., & Brady, M. (2015). Hypertrophic cardiomyopathy: a review. Anesthesia & Analgesia, 120(3), 554-569.
• Ingwall, J. S., & Weiss, R. G. (2004). Is the failing heart energy starved? On using chemical energy to support cardiac function. Circulation Research, 95(2), 135-145.
• Karwi, Q. G., Uddin, G. M., Ho, K. L., & Lopaschuk, G. D. (2018). Loss of metabolic flexibility in the failing heart. Frontiers in Cardiovascular Medicine, 5, 68.
• Karwi, Q. G., Zhang, L., Altamimi, T. R., Wagg, C. S., Patel, V., Uddin, G. M., Joerg, A. R., Padwal, R. S., Johnstone, D. E., Sharma, A., Oudit, G. Y., & Lopaschuk, G. D. (2019). Weight loss enhances cardiac energy metabolism and function in heart failure associated with obesity. Diabetes, Obesity and Metabolism, 21(8), 1944-1955.
• Knowlton, A. A., Chen, L., & Malik, Z. A. (2014). Heart failure and mitochondrial dysfunction: the role of mitochondrial fission/fusion abnormalities and new therapeutic strategies. Journal of Cardiovascular Pharmacology, 63(3), 196-206.
• Kumar, A. A., Kelly, D. P., & Chirinos, J. A. (2019). Mitochondrial dysfunction in heart failure with preserved ejection fraction. Circulation, 139(11), 1435-1450.
• Lopaschuk, G. D., Karwi, Q. G., Tian, R., Wende, A. R., & Abel, E. D. (2021). Cardiac energy metabolism in heart failure. Circulation Research, 128(10), 1487-1513.
• Lopaschuk, G. D., Ussher, J. R., Folmes, C. D., Jaswal, J. S., & Stanley, W. C. (2010). Myocardial fatty acid metabolism in health and disease. Physiological Reviews, 90(1), 207-258.
• Sanbe, A. (2013). Dilated cardiomyopathy: a disease of the myocardium. Biological and Pharmaceutical Bulletin, 36(1), 18-22.
• Shimokawa, J., Yokoshiki, H., & Tsutsui, H. (2007). Impaired activation of ATP-sensitive K+ channels in endocardial myocytes from left ventricular hypertrophy. American Journal of Physiology-Heart and Circulatory Physiology, 293(6), H3643-H3649.
• Tian, R., Colucci, W. S., Arany, Z., Bachschmid, M. M., Ballinger, S. W., Boudina, S., Bruce, J. E., & Dorn, G. W. (2019). Unlocking the secrets of mitochondria in the cardiovascular system: path to a cure in heart failure—a report from the 2018 National Heart, Lung, and Blood Institute Workshop. Circulation, 140(14), 1205-1216.
• Tong, M., Zablocki, D., & Sadoshima, J. (2020). The role of Drp1 in mitophagy and cell death in the heart. Journal of Molecular and Cellular Cardiology, 142, 138-145.
• Vakrou, S., & Abraham, M. R. (2014). Hypertrophic cardiomyopathy: a heart in need of an energy bar? Frontiers in Physiology, 5, 309.
• Yamada, S., Kane, G. C., Behfar, A., Liu, X. K., Dyer, R. B., Faustino, R. S., Miki, T., Seino, S., & Terzic, A. (2006). Protection conferred by myocardial ATP‐sensitive K+ channels in pressure overload‐induced congestive heart failure revealed in KCNJ11 Kir6. 2‐null mutant. The Journal of Physiology, 577(3), 1053-1065.
• Zhou, B., & Tian, R. (2018). Mitochondrial dysfunction in pathophysiology of heart failure. The Journal of Clinical Investigation, 128(9), 3716-3726.