In mice reprogramming of energy metabolism restores cardiac function after infarction
重新小鼠中的能量代指令序列，於梗塞後恢了心功能。
After birth, the human heart loses its regenerative capacity almost completely. Damage to the heart muscle, e.g. due to a heart attack, therefore usually leads to a permanent loss of function in adults.
於出生後，人心乎完全失再生能力。譬如，由於心病作，心肌造成。因此，通常於多成人中，致永久性功能失。
Scientists from the Max Planck Institute for Heart and Lung Research have now shown for the first time in mice that a change in the energy metabolism of heart muscle cells enables heart regeneration. In the animals, heart function could thus be restored to a large extent after a heart attack. The study is groundbreaking and could enable completely new therapeutic approaches.
目前，自德克斯普朗克心肺研究所的科家，在小鼠中，已首度，於心肌胞能量代上的改，能使心再生。在物中，心病作後，因此心功能，可能大程度被恢。研究具性，因此可能完全，新的治方法。
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1. 在具有Cpt1b基因不活的小鼠中，在梗塞後，心能再生。
In mice with an inactive Cpt1b gene, the heart can regenerate after an infarction.
Shortly after birth, the human heart largely loses its ability to repair itself in the event of damage. Injuries or diseases of the heart muscle therefore lead to permanent damage and a reduction in heart function. The loss of regenerative capacity is due, among other things, to the loss of the ability of heart muscle cells to divide after birth.
出生後不久，在受事件程中，人的心大部分失自行修能力。因此，心肌或疾病致，永久性及心功能下降。失再生能力的其他中，是由於在出生後，失心肌胞分裂能力。
This is accompanied by a fundamental change in the energy metabolism of the heart cells: Instead of obtaining energy from sugars, which is known as glycolysis, the heart muscle cells now obtain their energy largely from fats. This form of energy production is known as fatty acid oxidation.
伴著，心胞能量代的一根本改：在心肌胞大部分，脂肪取能量，而不是被通糖解的糖取能量。能量生的方式，被通脂肪酸氧化。
The research group led by Thomas Braun, Director at the Max Planck Institute for Heart and Lung Research in Bad Nauheim, Germany, started looking for new methods to promote heart regeneration:
由德克斯普朗克心肺研究所(位於巴特瑙海姆市)所，Thomas Braun的研究始找了，促心再生的新方法：
"It is known that animal species capable of regenerating their hearts primarily use sugars and glycolysis as fuel for heart muscle cells. The human heart also primarily uses glycolysis in early stages of development, but then switches to fatty acid oxidation because it can produce more energy," explain Xiang Li and Xuejun Yuan, authors of the study. "With the switch in energy production after birth, the activity of many genes changes and cell division activity is lost.
研究撰文人，Xiang Li及Xuejun Yuan解：「所周知，能再生心的物物，主要使用糖及糖解，作心肌胞的料。在育初期段中，人心主要也使用糖解。不，之後向脂肪酸氧化。因，它可以生更多能量。於出生後，著能量生上的，多基因的活性生改，果失胞分裂活力。
Individual metabolites from energy production also have important functions for the activity of enzymes that regulate gene activities. We therefore hoped to trigger changes in gene activities by reprogramming energy metabolism to turn cell division ability back on in cardiac muscle cells."
自能量生的各代物，於基因活性的酵素活性，也具有多重要功能。因此我期盼，藉由重新能量新代指令序列，以在基因活性上的改，重新心肌胞的胞分裂能力。」
To do this, the Max Planck researchers first inactivated a gene called Cpt1b, which is essential for fatty acid oxidation, in mice. "We then observed that hearts in these mice started to grow again," Li explains. Over the course of the experiment, cell numbers in the hearts of these mice nearly doubled.
此，克斯普朗克的研究人首先化了，於小鼠中一，於脂肪酸氧化至重要，被Cpt1b的基因。Li解：「之後，我察到，於此些老鼠中的心，再次始生。」在此程中，於此些小鼠的心中，胞量乎倍增。
In the next step, the Bad Nauheim researchers triggered heart attacks in mice in which Cpt1b was switched off. In the chosen approach, a phase of lack of blood flow to the heart is followed by a reperfusion phase, in which the heart is flushed again with oxygenated blood.
在接下一的步中，於巴特瑙海姆市(Bad Nauheim)的研究人，在Cpt1b被的小鼠中，了心病作。在被的方法中，心血流不足段，之後是再灌注段。在此段，心再次流充氧的血液。
"This model is comparable to a cardiac patient whose heart is treated with the insertion of a stent due to an occlusion of the coronary arteries," Yuan explains. The effect was impressive: otherwise common scars in the heart muscle were barely noticeable after weeks, and contractility in animals without Cpt1b almost returned to pre-infarction levels.
Yuan解：「模型似心病患者，由於冠阻塞，其心由使用插入支架的治。」此效果令人印象深刻：除此之外，於後，在心肌中常的疤痕乎不明，且在有Cpt1b 之物中的收力，乎恢到梗塞前的水平。
In further studies, the scientists were able to decipher the underlying mechanism: "In heart muscle cells of the mice with the inactivated gene, we found a twenty-fold increased level of alpha-ketoglutarate. The high level of this metabolite leads to a significant increase in the activity of the enzyme KDM5," Braun explains.
在多一步的研究中，此些科家能破解在的制：Braun解：「在此些具上述化之基因小鼠的心肌胞中，我了，α-酮戊二酸的含量增加二十倍。代物的高水平，致了在KDM5酶的活性上，著增加。」
This enzyme is a so-called histone demethylase, which removes methyl groups from histones and thus reduces the activity of various genes. The change in gene activity causes cardiac muscle cells to become immature and thus regain the ability to regenerate.
此酶是一，蛋白移除甲基，而降低各基因活性，所的蛋白去甲基化酶。此基因活性的化，致心肌胞得不成熟，因此重新得再生能力。
Braun sees the study as a real breakthrough: "By reprogramming the metabolism, we double the number of heart muscle cells, and after an infarction, heart function is almost completely restored."
Braun，研究是一真正的突破：「藉由重新新代的指令序列，我倍增了心肌胞的量，且在梗塞後，乎完全恢心功能。」
In addition, it is possible in principle to pharmacologically block the activity of the enzyme CPT1B -the gene product of Cpt1b. The development of an inhibitor that can be used to affect the activity of the CPT1B enzyme is the next step on the road to developing a therapy that may eventually be used in humans.
此外基本上，理上阻CPT1B酶(Cpt1b的基因物)的活性，是可能的。一能被用影CPT1B酶活性之抑制的，是在一，最可能被用於人法道路上的下一步。
However, Yuan and Braun emphasize, "We still have a long way to go before reliable treatments in humans become possible. The implementation of new findings from basic research is lengthy and expensive and is often accompanied by many unexpected problems. Nevertheless, we are confident that we will be able to therapeutically stimulate the regenerative capacity of the heart in the future."
不，Yuan及Braun：「在於人的可靠治法成可能之前，我仍有漫的路。自基研究之新的行，是漫且花高昂的。因此常伴多意想不到的。管如此，我有信心，於未能治性刺激心的再生能力。」
址：https://www.mpg.de/20981292/1020-pfor-cardiac-regeneration-becomes-possible-through-reprogramming-of-cell-metabolism-149770-x?c=2249
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