Effect of TFAM on ATP content in tachypacing primary cultured cardiomyocytes and atrial fibrillation patients.

Atrial fibrillation (AF) is one of the most common types of arrhythmia worldwide; although a number of theories have been proposed to explain the mechanisms of AF, the treatment of AF is far from satisfactory. Energy metabolism is associated with the development of AF. Mitochondrial transcription factor A (TFAM) serves a role in the maintenance and transcription of mitochondrial DNA. The present study aimed to investigate the association between TFAM and AF and the effect of TFAM on ATP content in cardiomyocytes. Left atrial appendage tissues were collected from 20 patients with normal sinus rhythm (SR) and 20 patients with AF, and the expression levels of TFAM in SR and AF tissues were evaluated. In addition, a tachypacing model of primary cultured cardiomyocytes was constructed to assess ATP content, cell viability and expression levels of TFAM, mitochondrially encoded (MT)‑NADH dehydrogenase 1 (ND1), MT‑cytochrome c oxidase 1 (CO1), NADH ubiquinone oxidoreductase core subunit 1 (NDUFS1) and cytochrome c oxidase subunit 6C (COX6C). Finally, the effects of overexpression and inhibition of TFAM on ATP content, cell viability and the expression levels of MT‑ND1 and MT‑CO1 were investigated. The expression levels of TFAM were decreased in AF tissues compared with SR tissues (P 0.05). Overexpression of TFAM increased ATP content, cell viability and expression levels of MT‑ND1 and MT‑CO1 (P<0.05). The inhibition of TFAM decreased ATP content, cell viability and expression levels of MT‑ND1 and MT‑CO1 (P<0.05). In summary, the results of the present study demonstrated that the expression levels of TFAM were decreased in AF tissues and tachypacing cardiomyocytes and that the restoration of TFAM increased the ATP content by upregulating the expression levels of MT‑ND1 and MT‑CO1 in tachypacing cardiomyocytes. Thus, TFAM may be a novel beneficial target for treatment of patients with AF.