Heart failure is characterized by the functional loss of ventricular contractility. It occurs following hypertrophy and ventricle deterioration resulting from cardiomyocyte apoptosis. 1 An early component of cardiomyocyte apoptosis in heart failure is the dysregulation of mitochondrial fission and fusion. [2][3][4][5][6][7] The relative rates of fusion and fission are normally tightly controlled, but during apoptosis, there is a dysregulation of key regulatory proteins like MFF, MFN1, MFN2, OPA1 and Drp1. 8 Much work has focused on characterizing the regulatory pathways governing mitochondrial fission and fusion in terms of how they become dysregulated in heart failure and in terms of identifying molecular targets for potentially blocking this dysregulation.MicroRNAs have gained significant attention as modulators of mitochondrial fission and fusion. MicroRNAs are endogenous, single-stranded, short RNA sequences (~22 nucleotides) that regulate target gene expression by binding to the 3' untranslated regions (UTRs) of target mRNAs. 9 The microRNAs miRNA-499, miRNA-140 and miRNA-30c have been shown to modulate mitochondrial fission

The kidney serves a central role in the control of blood pressure through the release of vasoactive substances and the urinary excretion of Na+. Patients with essential hypertension usually exhibit persistent high blood pressure accompanied by Na+ retention. L-dihydroxyphenylalanine (L‑DOPA) is an amino acid, converted by the enzyme aromatic L‑amino acid decarboxylase to dopamine. The uptake of L‑DOPA by cells of the proximal tubular epithelium of the kidney is controlled by the L‑type amino acid transporter 2 (LAT2). LAT2 belongs to the solute carrier family 7 (SLC7) of amino acid transporters and is coded by the SLC7A8 gene. SLC7A8 expression is increased in the second‑order mesenteric arteries and kidneys of spontaneously hypertensive rats. The present study aimed to investigate the physiological role of the SLC7A8 gene in L‑DOPA handling by kidney cells. Selective upregulation of SLC7A8 mRNA and protein levels was achieved by adenoviral transduction of NRK‑52E cells, which retain several properties of proximal tubular epithelial cells. In addition, L‑DOPA uptake was determined using high performance liquid chromatography; NRK‑52E cells expressing SLC7A8 exhibited increased uptake of L‑DOPA. The results of the present study suggested that SLC7A8 may serve a critical role in blood pressure control through regulating L‑DOPA uptake in renal epithelial cells of the proximal tubule.