Popovici D, Mihai N, Urbanavicius V
Endocrinologie. 1980 Jul-Sep;18(3):143-7.
ATP synthesis requires the presence of thyroid hormones that activate oxidative phosphorylation. ATP supports the energy consuming reactions such as actin-myosin interaction, calcium and sodium pump, which are essential in a normal heart function. Thyroid insufficiency depresses mitochondrial oxidation, leading to ATP depletion which can not be compensated by activated glycolysis. Glycolysis under conditions of hypoxia due to accumulation of lactate or NADPH, impairs membrane permeability and mitochondrial function, causing enzyme release and pump failure. In severe hyperthyroidism an ATP deficiency occurs by uncoupling of oxidative phosphorylation, T4 stimulating the extra-mitochondrial metabolic pathways. There is a disproportion between consumption of O2 and nutrients and ATP production. The T4--T3 excess via trace metal (magnesium, copper, zinc, iron, etc.) chelation inhibits enzyme activity which had impaired ATP synthesis. At the same time the excess of T4 by stimulating ATP-ase causes heat release and dissipation of ATP, favouring cardiothyreosis.
ATP合成需要甲状腺激素的存在，甲状腺激素可激活氧化磷酸化。ATP支持能量消耗反应，如肌动蛋白-肌球蛋白相互作用、钙泵和钠泵，这些对正常心脏功能至关重要。甲状腺功能不全抑制线粒体氧化，导致ATP耗竭，而激活的糖酵解无法补偿这种耗竭。由于乳酸或NADPH积累导致缺氧时，糖酵解会损害膜通透性和线粒体功能，导致酶释放和泵功能衰竭。在严重甲亢时，氧化磷酸化解偶联会导致ATP缺乏，T4刺激线粒体外代谢途径。氧气和营养物质的消耗与ATP产生之间存在失衡。通过微量金属（镁、铜、锌、铁等）螯合导致的T4-T3过量会抑制酶活性，从而损害ATP合成。同时，过量的T4通过刺激ATP酶导致热量释放和ATP消耗，促进甲状腺毒症性心脏病。
