Research press release


Nature Communications

Health: Understanding how fever affects heart function



今回、Glenn Fishmanたちは、電気信号に対する興奮性細胞(例えば、心筋)の応答を調節することが知られた繊維芽細胞増殖因子相同因子-2(FHF2)というタンパク質を特異的に欠損した遺伝子組み換えマウスを作製した。この変異マウスは、深部体温が摂氏37度で正常な心臓リズムを示したが、深部体温を摂氏3度上昇させると、心臓の電気伝導系が機能不全を起こし、心拍数が致命的なレベルまで徐々に減少した。そして、Fishmanたちは、正常な体温(平熱)に戻せば、この症状が完全に回復することを実証し、この心筋細胞の興奮に対する温度感受性抑制の背後にある機構がナトリウムチャネルの不活性化の変化であることを明らかにした。


A key regulator of heart cell electrical signals that protects against irregular heart rhythm arising in fever, is described in in a mouse study published in Nature Communications this week. The paper suggests that, in the future, therapies developed to target the protein could be used to help control heart rhythm when body temperature increases.

Fever commonly develops as part of body’s defense system against infection. Although providing a survival benefit, fever may also adversely affect the function of excitable tissues, such as the brain and heart causing seizures or life-threatening changes in heart rhythm (arrhythmia).

Glenn Fishman and colleagues genetically modified mice to lack a specific protein - fibroblast growth factor homologous factor 2 (FHF2) - that is known to modulate the response of excitable cells, such as cardiac muscle, to electrical signals. They find the mutant mice show normal heart rhythm at 37°C, but that increasing their core body temperature by as little as 3°C causes progressive and life-threatening deceleration of heart beats, due to failure of the heart’s electrical conduction system. They show this condition is fully reversible upon return to normal body temperature, or normothermia. The authors identify altered sodium channel inactivation as the mechanism behind this temperature-sensitive block of cardiomyocyte excitation.

They suggest that their data may also provide potential mechanistic connections between fever-induced arrhythmia and fever-induced epilepsy.

doi: 10.1038/ncomms12966

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