Mice lacking fat storage-inducing transmembrane protein 2 show improved profiles upon pressure overload-induced heart failure

Natsumi Nishihama, Takahiro Nagayama, Shinji Makino, Ryuta Koishi

Research output: Contribution to journalArticle

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.

Original languageEnglish
Article numbere01292
JournalHeliyon
Volume5
Issue number3
DOIs
Publication statusPublished - 2019 Mar 1

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Heart Failure
Pressure
Sarcoplasmic Reticulum
mouse FIT2 protein
Knockout Mice
Endoplasmic Reticulum
Skeletal Muscle
Proteins
Fats
Body Weight

Keywords

  • Cardiology
  • Physiology

ASJC Scopus subject areas

  • General

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Mice lacking fat storage-inducing transmembrane protein 2 show improved profiles upon pressure overload-induced heart failure. / Nishihama, Natsumi; Nagayama, Takahiro; Makino, Shinji; Koishi, Ryuta.

In: Heliyon, Vol. 5, No. 3, e01292, 01.03.2019.

Research output: Contribution to journalArticle

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