Objective To examine the regulatory relationship between the tensin 1 (TNS1) gene and miR-574-5p in cardiac arrest, assess its clinical significance, and verify the therapeutic potential of targeted inhibition of miR-574-5p. Methods Oxygen-glucose deprivation /reoxygenation (OGD/ R) cardiomyocyte and mouse asphyxia cardiac arrest / cardiopulmonary resuscitation (ACA/ CPR) models were established. Expression levels of miR-574-5p and TNS1 were detected by RT-qPCR. Protein expression levels of TNS1 in cardiomyocytes were detected by Western blot. The targeting relationship between miR-574-5p and TNS1 was verified by dual-luciferase reporter gene assay. Cell viability was detected by Cell Counting Kit-8 assay, and apoptosis was measured by flow cytometry. Serum levels of the cardiac injury marker cardiac troponin I ( cTnI ) and the oxidative stress markers malondialdehyde and 4-hydroxynonenal were detected by enzyme-linked immunosorbent assay. The cardiac function indices dp / dtmin and dp /dtmax were evaluated using a hemodynamic monitoring system, and cardiac function parameters, including left ventricular ejection fraction and left ventricular fractional shortening, were determined by echocardiography. ResultsOGD/ R treatment significantly upregulated the expression of miR-574-5p and inhibited the mRNA and protein expression of TNS1 in cardiomyocytes, while inhibition of miR-574-5p improved cardiomyocyte survival and alleviated oxidative stress injury (P<0. 05). In the ACA/ CPR model, cardiac function indices were significantly improved (P<0. 05), cardiac injury and oxidative stress markers were reduced (P<0. 05), and the upregulation of miR-574-5p and downregulation of TNS1 expression patterns in myocardial tissues were reversed in the miR-574-5p antagonist group (P<0. 05). Conclusions This study confirmed that targeted inhibition of miR-574-5p can improve cardiac function by upregulating the expression of TNS1, providing a new therapeutic target for myocardial protection after cardiac arrest.