Difference between revisions of "Team:SMMU-China/Description"

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<h2 class="inner-h">References</h2>
 
<h2 class="inner-h">References</h2>
 
<ol>
 
<ol>
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<li>W. Chen et al., Outline of the report on cardiovascular diseases in China, 2014. 18, F2 (2016).</li>
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<li>Johnson, F. L. "Pathophysiology and etiology of heart failure." Cardiology Clinics 32.1(2014):9-19.</li>
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<li>B. Ziaeian, G. C. J. N. R. C. Fonarow, Epidemiology and aetiology of heart failure. 13, 368 (2016).</li>
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<li>Smith, J. Gustav. "Molecular Epidemiology of Heart Failure: Translational Challenges and Opportunities." Jacc Basic to Translational Science2.6(2017):757-769.</li>
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<li>C. W. Yancy et al., 2016 ACC/AHA/HFSA Focused Update on New Pharmacological Therapy for Heart Failure: An Update of the 2013 ACCF/AHA Guideline for the Management of Heart Failure. 68, 1476-1488 (2016).</li>
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<li>Eschenhagen, T. "Is ryanodine receptor phosphorylation key to the fight or flight response and heart failure?." Journal of Clinical Investigation120.12(2010):4197-4203. Ullrich, Nina D., H. H. Valdivia, and E. Niggli. "PKA phosphorylation of cardiac ryanodine receptor modulates SR luminal Ca2+ sensitivity." Journal of Molecular & Cellular Cardiology 53.1(2012):33-42.</li>
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<li>J. S. Hulot, K. Ishikawa, R. J. J. E. H. J. Hajjar, Gene therapy for the treatment of heart failure: promise postponed. 37, 1651-1658 (2016).</li>
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<li>Marx, S. O., et al. "PKA Phosphorylation Dissociates FKBP12.6 from the Calcium Release Channel (Ryanodine Receptor)." Cell 101.4(2000):365-376.</li>
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<li>M. Luo, M. E. J. C. R. Anderson, Mechanisms of Altered Ca^2^+ Handling in Heart Failure. 113, 690-708 (2013).</li>
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<li>Menzel, S., et al. "Nanobody-Based Biologics for Modulating Purinergic Signaling in Inflammation and Immunity." Frontiers in Pharmacology9(2018):266.</li>
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<li>F. V. J. J. o. B. C. Petegem, Ryanodine Receptors: Structure and Function. 287, 31624-31632 (2012).</li>
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<li>Wikipedia. Single-domain antibody. https://en.wikipedia.org/wiki/Single-domain_antibody.</li>
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<li>G. W. Cho, F. Altamirano, J. A. J. B.-M. B. o. D. Hill, Chronic heart failure: Ca2+, catabolism, and catastrophic cell death. 1862, 763-777 (2016).</li>
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<li>Wikipedia. Phage display. https://en.wikipedia.org/wiki/Phage_display.</li>
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<li>J. Roussel et al., Palmitoyl-carnitine increases RyR2 oxidation and sarcoplasmic reticulum Ca 2 + leak in cardiomyocytes: Role of adenine nucleotide translocase. 1852, 749-758 (2015).</li>
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<li>Ma, X., et al. "Therapeutic delivery of cyclin-A2 via recombinant adeno-associated virus serotype 9 restarts the myocardial cell cycle: an in vitro study." Molecular Medicine Reports 11.5(2015):3652-3658.</li>
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<li>M. Munkvik et al., Training effects on skeletal muscle calcium handling in human chronic heart failure. 42, 847-855 (2010).</li>
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Revision as of 16:17, 8 October 2018

1 Heart failure
2 CaRTIN
References

Description

1 Heart failure

What is heart failure?

The main function of the heart is to pump blood, providing power to promote blood circulation to meet the metabolic needs of tissue cells throughout the body.

Heart failure is when the heart's systolic or diastolic function declines, resulting in a failure of cardiac output to meet the body's metabolic needs. Heart failure is the severe and terminal stage of various heart diseases. According to the patients at all stages, patients including hypertension, coronary heart disease and diabetes are at risk of heart failure.

Figure 1

Clinical status and influence of heart failure

The global incidence of chronic heart failure is 3 percent among adults and as high as 10 percent over the age of 80, according to the study. Death rates from heart failure have increased six fold over the past 40 years, and about 60 percent of patients die within five years of being diagnosed, with a five-year survival rate similar to that of malignant tumors. Heart failure also brings huge economic burden to society. In Europe and North America, the hospitalization of heart failure accounts for 1% to 4% of the hospitalization quantity, and 46% of the discharged patients are re-admitted due to the worsening of heart failure in 2 months. The average hospitalization time is 5-10 days, accounting for a large amount of medical resources, and the cost of heart failure treatment accounts for 1% to 2% of the total medical expenditure. The United States spent about $39.3 billion on heart failure in 2010, and total spending on patients with heart failure is expected to increase by 50-100% over the next 10 years. At the same time, as the end-stage patients of heart failure lose their activity and work capacity, the side effects are also very large, resulting in a huge family burden.

Figure 2

2 CaRTIN

What is RyR2? What is it made up of?

As we have introduced before, Calcium (Ca2+) is the important physiological ligand that activates the channels in cardiac muscle during excitation-contraction (EC) coupling. The heart dysfunction will happen when Ca2+ cycle is in a mess, which in the end leads to heart failure. That’s why we have to mention the Ca2+ release channels (a kind of ryanodine receptor) on the sarcoplasmic reticulum (SR) of striated muscles. They adjust and control Ca2+ between cytoplasm and SR as a biphasic channel such that low cytosolic [Ca2+] (mM) activates the channels and high cystolic [Ca2+] (mM) inactivates the channels, confirming their crucial role in EC coupling. In cardiac muscle, the Calcium release channels on the SR is named as the type 2 ryanodine receptor (RyR2). It is a tetramer comprised of four 565,000 Dalton RyR2 polypeptides and four 12,000 Dalton FK-506 binding proteins (FKBP12.6).

References

  1. Johnson, F. L. "Pathophysiology and etiology of heart failure." Cardiology Clinics 32.1(2014):9-19.
  2. Smith, J. Gustav. "Molecular Epidemiology of Heart Failure: Translational Challenges and Opportunities." Jacc Basic to Translational Science2.6(2017):757-769.
  3. Eschenhagen, T. "Is ryanodine receptor phosphorylation key to the fight or flight response and heart failure?." Journal of Clinical Investigation120.12(2010):4197-4203. Ullrich, Nina D., H. H. Valdivia, and E. Niggli. "PKA phosphorylation of cardiac ryanodine receptor modulates SR luminal Ca2+ sensitivity." Journal of Molecular & Cellular Cardiology 53.1(2012):33-42.
  4. Marx, S. O., et al. "PKA Phosphorylation Dissociates FKBP12.6 from the Calcium Release Channel (Ryanodine Receptor)." Cell 101.4(2000):365-376.
  5. Menzel, S., et al. "Nanobody-Based Biologics for Modulating Purinergic Signaling in Inflammation and Immunity." Frontiers in Pharmacology9(2018):266.
  6. Wikipedia. Single-domain antibody. https://en.wikipedia.org/wiki/Single-domain_antibody.
  7. Wikipedia. Phage display. https://en.wikipedia.org/wiki/Phage_display.
  8. Ma, X., et al. "Therapeutic delivery of cyclin-A2 via recombinant adeno-associated virus serotype 9 restarts the myocardial cell cycle: an in vitro study." Molecular Medicine Reports 11.5(2015):3652-3658.
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