Abstract
Fat storage-inducing transmembrane proteins 1 and 2 (FITM1 and FITM2, respectively) are transmembrane endoplasmic/sarcoplasmic reticulum proteins involved in lipid droplet formation. The physiological functions of FITM1 have only been reported in skeletal muscle, while those of FITM2 were analyzed using genetically engineered mice. However, their roles in the heart have not been characterized. To examine their cardiac functions, we analyzed Fitm1- or Fitm2-knockout mice. Neither constitutive Fitm1 (−/−) aged nor heart failure model mice showed significant differences in heart size or function. Fitm2 (−/−) mice exhibited embryonic death, and aged Fitm2 (+/−) mice had shortened left ventricular end-diastolic dimension, and shortened left ventricular end-systolic dimension. However, body weight and ejection fraction of Fitm2 (+/−) mice were similar to those of wild-type littermates. In the chronic heart failure models, Fitm2 (+/−) mice showed significant suppression of increased left ventricular end-diastolic dimension and reduced ejection fraction. These results suggest the involvement of Fitm2 in chronic heart failure, whereas Fitm1 have a minor effect in this context in mice.
Highlights
Fat storage-inducing transmembrane proteins 1 and 2 (FITM1 and FITM2, respectively) are members of a conserved gene family that are important for lipid droplet accumulation [1, 2, 3]
Our findings collectively suggest that downregulation of Fitm, especially Fitm2 expression or function may have a beneficial effect in patients with heart failure
For the chronic heart failure model induced by myocardial infarction (MI), the chest cavity was exposed by cutting the intercostal muscle, and the left coronary artery was subsequently ligated with a 7e0 silk suture
Summary
Fat storage-inducing transmembrane proteins 1 and 2 (FITM1 and FITM2, respectively) are members of a conserved gene family that are important for lipid droplet accumulation [1, 2, 3]. We found that these proteins were identified in mice and/or human heart samples by proteomic analysis, affected the cardiovascular system and body development in zebrafish, and that their modulated expression or function can change lipid droplet formation, ER function, and cellular metabolism in cells [9]. These data suggested their potential to modulate heart failure pathogenesis. Our findings collectively suggest that downregulation of Fitm, especially Fitm expression or function may have a beneficial effect in patients with heart failure
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