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Biophysical Reviews

, Volume 11, Issue 2, pp 241–244 | Cite as

A step towards understanding the molecular nature of human heart failure: advances using the Sydney Heart Bank collection

  • Amy Li
  • Sean Lal
  • Cristobal G. dos RemediosEmail author
Commentary

The Sydney Heart Bank (SHB) primarily contains tissues from hearts that were either derived from patients undergoing an isotopic heart transplantation or were from non-failing donor hearts. The latter had no apparent disease but were not required or not suitable for transplantation. Several review articles have been written (dos Remedios et al. 2017, 2018; Lal et al. 2015; Li et al. 2013), but none has attempted to summarise all causes of the failing hearts in the SHB. This review gathers the relevant information about the heart tissue from 450 patients with cardiomyopathies and 120 healthy donor hearts.

Our aim is to give readers the ability to assess whether the SHB contains tissue that might be useful for proposed experiments, particularly where prospective users have preliminary data based on animal models of human heart failure. We are often contacted by researchers who have data from failing or diseased human heart tissue but have no access to healthy donors. Few realise that the...

Notes

Compliance with ethical standards

Conflict of interest

Amy Li declares that she has no conflict of interest. Sean Lal declares that he has no conflict of interest. Cristobal G. dos Remedios declares that he has no conflict of interest.

Ethical approval

This article does not contain any studies with human participants or animals performed by any of the authors.

Supplementary material

12551_2019_514_MOESM1_ESM.docx (79 kb)
ESM 1 (DOCX 79 kb)

References

  1. Bayliss CR, Jacques AM, Leung MC, Ward DG, Redwood CS et al (2013) Myofibrillar Ca2+−sensitivity is uncoupled from troponin I phosphorylation in hypertrophic obstructive cardiomyopathy due to abnormal troponin T. Cardiovasc Res 97:500–508CrossRefGoogle Scholar
  2. Bennett PM (2018) Riding the waves of the intercalated disc of the heart. Biophys Rev 10:955–959.  https://doi.org/10.1007/s12551-018-0438-z CrossRefGoogle Scholar
  3. Bergmann O, Zdunek S, Felker A, Salehpour M, Alkass K et al (2015) Dynamics of cell generation and turnover in the human heart. Cell 161:1566–1575.  https://doi.org/10.1016/j.cell.2015.05.026 CrossRefGoogle Scholar
  4. dos Remedios CG, Lal SP, Li A, McNamara J, Keogh A et al (2017) The Sydney Heart Bank: improving translational research while eliminating or reducing the use of animal models of human heart disease. Biophys Rev 9:431–441.  https://doi.org/10.1007/s12551-017-0305-3 CrossRefGoogle Scholar
  5. dos Remedios CG, Li A, Lal S (2018) Non-sarcomeric causes of Heart failure: a Sydney Heart Bank perspective. Biophys Rev 10(4):949–954.  https://doi.org/10.1007/s12551-018-0441-4
  6. Gehmlich L, Ehler E (2018) Non-sarcomeric causes of heart failure. Biophys Rev 10:943–947.  https://doi.org/10.1007/s12551-018-0444-1 CrossRefGoogle Scholar
  7. Huang Z-P, Ding Y, Chen J, Wu G, Kataoka M, Hu Y, Yang J-H, Liu J, Drakos SG, Selzman CH, Kyselovic J, Qu L-H, dos Remedios CG, Pu WT, Wang D-Z (2016) Long non-coding RNAs link extracellular matrix gene expression to ischemic cardiomyopathy. Cardiovasc Res 112:543–554.  https://doi.org/10.1093/cvr/cvw201 CrossRefGoogle Scholar
  8. Jin SC, Homsy J, Zaidi S, Lu Q, Morton S et al (2017) Contribution of rare inherited and de novo variants in 2,871 congenital heart disease probands. Nat Genet 49:1593–1601.  https://doi.org/10.1038/ng.3970 CrossRefGoogle Scholar
  9. Klauke B, Gaertner-Rommel A, Schulz U, Kassner A, Zu Knyphausen E et al (2017) High proportion of genetic cases in patients with advanced cardiomyopathy including a novel homozygous Plakophilin 2-gene mutation. PLoS One 12:e0189489.  https://doi.org/10.1371/journal.pone.0189489 CrossRefGoogle Scholar
  10. Kong SW, Hu Y, Ho J, Ikeda S, Polster S, John R, Hall JL, Bisping E, Pieske B, dos Remedios CG, Pu WT (2010) Heart failure associated changes in RNA splicing of sarcomere genes. Circ Cardiovasc Genet 3:138–146CrossRefGoogle Scholar
  11. Lal S, Li A, Allen D, Allen PD, Bannon P et al (2015) Best practice BioBanking of human heart tissue. Biophys Rev 7:399–406CrossRefGoogle Scholar
  12. Li A, Estigoy C, Raftery M, Cameron D, Odeberg J et al (2013) Heart research advances using database search engines, human protein atlas and the Sydney Heart Bank. Heart Lung Circ 22:819–826.  https://doi.org/10.1016/j.hlc.2013.06.006 CrossRefGoogle Scholar
  13. Lin Z, Guo H, Cao Y, Zohrabian S, Zhou P, Ma Q, VanDusen N, Guo Y, Zhang J, Stevens SM, Liang F, Quan Q, van Gorp PR, Li A, dos Remedios C, He A, Bezzerides VJ, Pu WT (2016) Acetylation of VGLL4 regulates hippo-YAP signaling and postnatal growth. Dev Cell 39:466–479.  https://doi.org/10.1016/j.devcel.2016.09.005 CrossRefGoogle Scholar
  14. Marston S, Montgiraud C, Munster AB, Copeland O, Onjee C et al (2015) OBSCN mutations associated with dilated cardiomyopathy and haploinsufficiency. PLoS One 10:e0138568.  https://doi.org/10.1371/journal.pone.0138568 CrossRefGoogle Scholar
  15. Messer AE, Bayliss CR, El-Mezgueldi M, Redwood CS, Ward DG et al (2016) Mutations in troponin T associated with hypertrophic cardiomyopathy increase Ca2+−sensitivity and suppress the modulation of Ca2+−sensitivity by troponin I phosphorylation. Arch Biochem Biophys 601:113–120.  https://doi.org/10.1016/j.abb.2016.03.027 CrossRefGoogle Scholar
  16. Mollova M, Bersell K, Walsh S, Savla J, Das LT et al (2013) Cardiomyocyte proliferation contributes to heart growth in young humans. Proc Natl Acad Sci U S A 110:1446–1451CrossRefGoogle Scholar
  17. Papadaki M, Vivhorev PG, Marston SB, Messer A (2015) Uncoupling of myofilament Ca2+−sensitivity from troponin I phosphorylation by mutations can be reversed by epigallocatechin-3-gallate. Cardiovasc Res 108:99–110.  https://doi.org/10.1093/cvr/cvv181 CrossRefGoogle Scholar
  18. Piroddi N, Witjas-Paalberends ER, Ferrara C, Ferrantini C, Vitale G et al (2019) The homozygous K280N troponin T mutation alters cross-bridge kinetics and energetics in human HCM. J Gen Physiol 151:18–29.  https://doi.org/10.1085/jgp.201812160 CrossRefGoogle Scholar
  19. Polizzotti BD, Ganapathy B, Walsh S, Choudhury S, Ammanamanchi N et al (2015) Stimulation of cardiomyocyte regeneration in neonatal mice and in human myocardium with neuregulin reveals a therapeutic window. Sci Translat Medic 7.  https://doi.org/10.1126/scitranslmed.aaa5171
  20. Sequeira V, Wijnker PJM, Nijenkamp LAM, Najafi A, Rosalie Witjas-Paalberends (2013) Perturbed length-dependent activation in human hypertrophic cardiomyopathy with sarcomere mutations in myosin and thin filament proteins. Circ Res 112:1491–1505Google Scholar
  21. Stroud MJ (2018) Linker of nucleoskeleton and cytoskeleton complex proteins in cardiomyopathy. Biophys Rev 10:1033–1051.  https://doi.org/10.1007/s1255-1-018-0431-6 CrossRefGoogle Scholar
  22. Witjas-Paalberends P, Tencate FJ, Michels M, Niessen JWM, Poggesi C et al (2013) Cellular dysfunction in hypertrophic cardiomyopathy. Cardiovasc Res 99:432–441CrossRefGoogle Scholar
  23. Witjas-Paalberends ER, Güçlü A, Germans T, Knaapen P, Harms HJ et al (2014) Gene-specific increase in energetic cost of contraction in hypertrophic cardiomyopathy caused by thick filament mutations. Cardiovasc Res 103:248–257CrossRefGoogle Scholar

Copyright information

© International Union for Pure and Applied Biophysics (IUPAB) and Springer-Verlag GmbH Germany, part of Springer Nature 2019

Authors and Affiliations

  1. 1.The University of SydneySydneyAustralia

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