| First Author | Nishihama N | Year | 2019 |
| Journal | Heliyon | Volume | 5 |
| Issue | 3 | Pages | e01292 |
| PubMed ID | 30923760 | Mgi Jnum | J:303195 |
| Mgi Id | MGI:6512094 | Doi | 10.1016/j.heliyon.2019.e01292 |
| Citation | Nishihama N, et al. (2019) Mice lacking fat storage-inducing transmembrane protein 2 show improved profiles upon pressure overload-induced heart failure. Heliyon 5(3):e01292 |
| abstractText | 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. |
