Abstract

Poster Presentations

Day 3, May 17（Wed.）　　Room P (Foyer, Room 1004-1007)

3P-23　　PDF

Multi-omics strategy for dissecting immunometabolism of Dilated Cardiomyopathy (DCM) on delta-sarcoglycan deficient hamster model

(¹Doshisha Univ., ²Shimadzu, ³Setsunan Univ., ⁴Kyoto Univ., ⁵NCVC, ⁶NCNP, ⁷Hokusetsu General Hosp.)
^oMaiko Okamura¹, Shinichi Yamaguchi², Takushi Yamamoto², Koji Okuda², Ryo Inoue³, Yuriko Teshima⁴, Keisuke Hakamada⁴, Inori Shintani¹, Takashi Tsuji⁴, Kisaki Amemiya⁵, Kenji Minatoya⁴, Hidetoshi Masumoto⁴, Satoru Noguchi⁶, Ichizo Nishino⁶, Hatsue Ueda^5,7, Masaya Ikegawa¹

Dilated cardiomyopathies (DCM) is a group of progressive, poor prognosis diseases that primarily consist of ventricular enlargement and myocardial contractile dysfunction. J2N-k hamsters (J2N-k), which have a defective δ-sarcoglycan (δ-SG) encoding gene, have been utilized as a suitable DCM animal model because the dilation of the ventricles and dysfunction was noticeable at about 20 weeks of age. Currently, the precise phenotypes of J2N-k on heart and skeletal muscles have not been elucidated. In our previous study, we have detected several cardiovascular pathological features of J2N-k heart including inflammation, fibrosis, bone formation and giant cell in the early to mid-stage of J2N-k hamsters. In order to answer what is the molecular mechanism underlying cardiac pathology of J2N-k hamsters, here we adopt and integrate multi-modal imaging mass spectrometry in terms of immunometabolism in a spatially and temporally resolved manner.