Clarification of novel sympathetic nerve-independent pathophysiological interactions between heart and brain in cardiac remodeling

2022 Fiscal Year Final Research Report

• Project/Area Number: 20K08506
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 53020:Cardiology-related
• Research Institution: National Cardiovascular Center Research Institute
• Principal Investigator: Otani Kentaro 国立研究開発法人国立循環器病研究センター, 研究所, 研究室長 (50470191)
• Project Period (FY): 2020-04-01 – 2023-03-31
• Keywords: 周産期心筋症 / ナトリウム利尿ペプチド / 心肥大 / 授乳 / 臓器連環

Outline of Final Research Achievements

We have demonstrated that mice lacking guanylyl cyclase-A (GC-A-KO), a receptor for atrial and brain natriuretic peptides, exhibit the severe postpartum cardiac hypertrophy and cardiac dysfunction like postpartum cardiomyopathy (PPCM). The elevated plasma aldosterone level in lactating GC-A-KO and the disappearance of lactation-induced cardiac hypertrophy in GC-A-KO by the inactivation of neural aldosterone receptor depict that the neural aldosterone system might be involved in the lactation-induced cardiac hypertrophy. However, the underlying mechanisms remains unclear. The aim of this study was to clarify the mechanisms of lactation-induced cardiac hypertrophy in GC-A-KO, especially focusing on the novel pathophysiological interactions between brain and heart.

Free Research Field

循環器内科学

Academic Significance and Societal Importance of the Research Achievements

周産期心筋症は心疾患既往のない女性が妊娠後期から産褥期にかけて心不全を発症し、拡張型心筋症に類似した病態を呈する疾患であり、疾患特異的な診断および治療法は未だ存在しない。これまでの一連の研究の結果、周産期心筋症の発症機序が少しずつ明らかになりつつある。今後、本研究成果を基にした周産期心筋症に対する疾患特異的な診断・治療法の開発が期待される。