運動がなぜ心臓疾患を改善し、予防するのかについて新たな理解が得られました。以下に、この研究の主なポイントと追加情報をまとめます。
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マイオネクチンの発見と作用機序:
- マイオネクチンは、骨格筋から分泌されるホルモンであり、有酸素運動によって増加します。
- 研究では、マイオネクチンが心臓を保護し、心筋梗塞などの心臓疾患の予防・治療を促進することが明らかになりました。
- マイオネクチンは、心筋組織内の細胞死と炎症反応を抑制し、心筋梗塞のサイズを縮小します。
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運動療法の重要性:
- 有酸素運動（例：ウォーキング）は、マイオネクチンの分泌を増加させ、心臓を保護する作用があります。
- 心筋梗塞や狭心症などの心臓疾患を予防するために、運動療法が推奨されます。
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マイオネクチンの医薬品への応用可能性:
- マイオネクチンは有酸素運動によって増加するため、このホルモンの働きを模倣する医薬品の開発が期待されます。
- これにより、運動の効果を得られない患者や、運動が困難な状況下でも心臓を保護することが可能になります。
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糖尿病と心臓疾患の関連:
- 研究によれば、糖尿病のある人は心臓疾患のリスクが増加します。したがって、糖尿病患者にとって特に運動療法の重要性が高まります。
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将来の展望:
- 今後の研究では、マイオネクチンのさらなる機能解明や、その他の心臓疾患への応用について探求されるでしょう。
- 運動と同等の効果をもたらす医薬品の開発には、より深い理解が必要ですが、その可能性は期待されます。
この研究は、心臓疾患に関する新たな治療法や予防法の開発に向けて、重要な基盤となる成果です。今後の研究や臨床応用に期待が寄せられます。
Here's the English translation of the provided text:
Understanding the Mechanism: Why Exercise is Beneficial, Revealing the Role of Muscle Hormones in Protecting the Heart
Keywords: Lifestyle, Diabetes Complications, Exercise Therapy
A study conducted by Nagoya University has revealed that hormones produced by skeletal muscles can protect the heart, thus promoting prevention and treatment of heart conditions such as myocardial infarction. It has been found that engaging in activities like walking can increase the production of these hormones.
Why Does Exercise Improve Heart Health?
The research highlights that hormones released from muscles play a role in safeguarding the heart, thereby aiding in the prevention and treatment of conditions like myocardial infarction. Heart disease ranks as the second leading cause of death among Japanese individuals, with ischemic heart diseases such as myocardial infarction being prominent. Particularly, individuals with diabetes face an increased risk of ischemic heart diseases, with reports indicating a 1.8 to 3 times higher risk. Measures are required to prevent and mitigate cardiovascular diseases, including arteriosclerosis and ischemic heart diseases, especially in individuals with diabetes.
Exercise therapy proves effective in preventing myocardial infarction and angina, with approximately 30 minutes of aerobic exercise like walking recommended daily. However, studies elucidating the effects of exercise at the molecular level remain scarce.
Recent research reveals that skeletal muscles, responsible for supporting and moving the body, also serve as endocrine organs capable of hormone production. Hormones secreted from skeletal muscles have been found to influence the pathophysiology of metabolic disorders like type 2 diabetes and cardiovascular diseases.
Related Information
- Complications of diabetes can be prevented by addressing five risk factors: a study of 300,000 individuals.
- Diabetes and hypertension warrant attention: guidelines from the Kidney Society on CKD Management 2018.
- Consuming eggs does not significantly affect blood sugar or cholesterol levels in individuals with diabetes.
- Myonectin, secreted from skeletal muscles, protects the heart.
The Cardioprotective Role of Myonectin
In this study, the research team focused on "myonectin," a hormone produced and secreted from skeletal muscles, which increases with aerobic endurance exercises like walking.
Using mice in experiments, the researchers observed that mice unable to produce myonectin showed increased myocardial infarction size and decreased heart function, along with exacerbated cell death and inflammatory reactions within cardiac muscle tissue, even after reopening occluded blood vessels. However, in mice capable of producing myonectin, aerobic exercise increased blood myonectin levels, suppressing cell death and inflammation within cardiac muscle tissue and reducing myocardial infarction size.
Conversely, myonectin-deficient mice did not experience protective effects against myocardial ischemia despite aerobic exercise. These findings demonstrate the anti-cell death and anti-inflammatory effects of myonectin, contributing to heart protection. Furthermore, it was shown that myonectin increases in the bloodstream through aerobic exercise, exerting protective effects on the heart.
Myonectin Increases Through Exercise
Myonectin is abundant only in skeletal muscles and is almost absent in cardiac muscle tissue. Administering myonectin systemically before the onset of myocardial ischemia was found to reduce myocardial infarction size compared to the control group.
The mechanism by which exercise therapy prevents myocardial infarction and angina involves the increase of myonectin secreted from skeletal muscles through aerobic exercise, which directly acts on cardiac muscle tissue, suppressing cell death and inflammatory reactions and exerting protective effects against ischemic heart diseases.
The research team also conducted cellular experiments. Adding myonectin to cultured cardiac muscle cells suppressed cell death induced by low oxygen/reoxygenation stimuli. Furthermore, myonectin suppressed the production of inflammatory proteins in macrophages, immune cells deeply involved in inflammation.
Hope for Drug Development with Effects Similar to Exercise
The research team believes that myonectin increases the secretion of physiological active substances that control inflammation and cell death and activates intracellular signals. By increasing the concentration of myonectin produced in skeletal muscles, the protective effect on the heart can be achieved.
Myonectin increases through aerobic exercise. Exercise therapy is necessary to increase the amount and improve the function of this hormone.
A more detailed understanding of myonectin's functions in the body could lead to elucidating the causes of cardiovascular diseases, including ischemic heart diseases controlled by aerobic exercise, in particular. Additionally, there is potential for developing drugs to prevent and treat cardiovascular diseases and drugs that exert effects similar to exercise.
The study was conducted by Professor Noriyuki Ota of the Department of Molecular Cardiovascular Medicine at Nagoya University Graduate School of Medicine, Professor Toyaki Murabara of Cardiovascular Internal Medicine, and their research team. Details are published in the scientific journal "Circulation Research."