Abstract
An essential procedure for the treatment of myocardial infarction is restoration of blood flow in the obstructed infarct artery, which may cause ischaemia/reperfusion (I/R) injury. Heart I/R injury manifests in oxidative stress, metabolic and morphological disorders, or cardiac contractile dysfunction. Klotho protein was found to be produced in the heart tissue and participate in antioxidation or ion homeostasis. The aim of this study was to examine an influence of Klotho protein on the heart subjected to I/R injury. Wistar rats served as a surrogate heart model ex vivo. Rat hearts perfused using the Langendorff method were subjected to global no-flow ischaemia, and isolated rat cardiomyocytes underwent chemical I/R in vitro, with or without recombinant Klotho protein administration. Haemodynamic parameters of heart function, cell contractility, markers of I/R injury and oxidative stress, and the level of contractile proteins such as myosin light chain 1 (MLC1) and troponin I (TnI) were measured. The treatment of hearts subjected to I/R injury with Klotho protein resulted in a recovery of heart mechanical function and ameliorated myocyte contractility. This improvement was associated with decreased tissue injury, enhanced antioxidant capacity, and reduced release of MLC1 and TnI. The present research showed the contribution of Klotho to cardioprevention during I/R. Thus, Klotho protein may support the protection from I/R injury and prevention of contractile dysfunction in the rat heart.
Highlights
Restoration of the flow in the obstructed infarct artery is pivotal for the treatment of myocardial infarction
Subjecting the isolated rat hearts to I/R protocol resulted in a significant decrease in cardiac haemodynamic parameters (Table 1, Figure 2)
Supplementation of aerobically perfused hearts with Klotho protein did not affect any of the measured parameters in comparison to the aero group (Table 1, Figure 2)
Summary
Restoration of the flow in the obstructed infarct artery is pivotal for the treatment of myocardial infarction. Revascularization and restoration of the blood flow inflict myocardial ischaemia/reperfusion (I/R) injury. It is known that I/R leads to oxidative stress and the subsequent cascade of pathophysiological events in the heart. The important factors contributing to the pathogenesis of I/R injury are the degradation of heart contractile proteins by proteolytic enzymes and necrotic cell death. The proteolytic enzymes like matrix metalloproteinases (MMPs) degrade cardiac troponin, titin, or myosin light chains (MLCs). The approach of regulating oxidative stress in the heart may support the reduction of maladaptive response established during I/R injury. Searching for new factors contributing to the prevention and treatment of myocardial injury following I/R is needed
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