Human cardiac myosin heavy chain isoforms in fetal and failing adult atria and ventricles
Abstract
The goal of this study was to test the hypothesis that the relative amounts of the cardiac myosin heavy chain (MHC) isoforms MHC-α and MHC-β change during development and transition to heart failure in the human myocardium. The relative amounts of MHC-α and MHC-β in ventricular and atrial samples from fetal (gestational days 47–110) and nonfailing and failing adult hearts were determined. The majority of the fetal right and left ventricular samples contained small relative amounts of MHC-α (mean < 5% of total MHC). There was a small significant decrease in the level of MHC-α in the ventricles between 7 and 12 wk of gestation. Fetal atria expressed predominantly MHC-α (mean > 95%), with MHC-β being detected in most samples. The majority of adult nonfailing right and left ventricular samples had detectable levels of MHC-α ranging from 1 to 10%. Failing right and left ventricles expressed a significantly lower level of MHC-α. MHC-α comprised ∼90% of the total MHC in adult nonfailing left atria, whereas the relative amount of MHC-α in the left atria of individuals with dilated or ischemic cardiomyopathy was ∼50%. The differences in MHC isoform composition between fetal and nonfailing adult atria and between fetal and nonfailing adult ventricles were not statistically significant. We concluded that the MHC isoform compositions of fetal human atria are the same as those of nonfailing adult atria and that the ventricular MHC isoform composition is different between adult nonfailing and failing hearts. Furthermore, the marked alteration in atrial MHC isoform composition, associated with cardiomyopathy, does not represent a regression to a pattern that is uniquely characteristic of the fetal stage.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The predominant myosin heavy chain isoform in sheep is slow beta-MHC (~100%), similar to humans (>90-95%).
“The predominate myosin heavy chain isoform is the slow β-MHC in sheep (~100%) similar to humans (>90–95%) (Hamilton & Ianuzzo, 1991; Miyata, et al., 2000; Reiser, et al., 2001).”
From Small and large animal models in cardiac contraction research: advantages and disadvantages (2014) · cites this paper as Reiser, et al., 2001
Cites
Molecular diversity of myofibrillar proteins: gene regulation and functional significance
Schiaffino, S., & Reggiani, C. (1996) · Physiological Reviews · doi:10.1152/physrev.1996.76.2.371 · Cited by 1,545 · see citing works
THE CELLULAR AND MOLECULAR RESPONSE OF CARDIAC MYOCYTES TO MECHANICAL STRESS
Sadoshima, J., & Izumo, S. (1997) · Annual Review of Physiology · doi:10.1146/annurev.physiol.59.1.551 · Cited by 868 · see citing works
Altered myocardial force-frequency relation in human heart failure.
Mulieri, L. A., Hasenfuss, G. P., Leavitt, B. J., Allen, P. D., & Alpert, N. R. (1992) · Circulation · doi:10.1161/01.cir.85.5.1743 · Cited by 597 · see citing works
Myosin heavy chain isoform expression in the failing and nonfailing human heart
Miyata, S., Minobe, W., Bristow, M. R., & Leinwand, L. A. (2000) · Circulation Research · doi:10.1161/01.res.86.4.386 · Cited by 538 · see citing works
Lowes, B. D., Minobe, W. A., Abraham, W. T., Rizeq, M. N., Bohlmeyer, T. J., Quaife, R. A., Roden, R. L., Dutcher, D. L., Robertson, A. D., Voelkel, N. F., et al. (1997) · Journal of Clinical Investigation · doi:10.1172/jci119770 · Cited by 496 · see citing works
Unloaded heart in vivo replicates fetal gene expression of cardiac hypertrophy
Depré, C., Shipley, G. L., Chen, W., Han, Q., Doenst, T., Moore, M. L. G., Stepkowski, S. M., Davies, P. J., & Taegtmeyer, H. (1998) · Nature Medicine · doi:10.1038/3253 · Cited by 423 · see citing works
Myosin heavy chain gene expression in human heart failure.
Nakao, K., Minobe, W. A., Roden, R. L., Bristow, M. R., & Leinwand, L. A. (1997) · Journal of Clinical Investigation · doi:10.1172/jci119776 · Cited by 413 · see citing works
THE MAMMALIAN MYOSIN HEAVY CHAIN GENE FAMILY
Weiss, A., & Leinwand, L. A. (1996) · Annual Review of Cell and Developmental Biology · doi:10.1146/annurev.cellbio.12.1.417 · Cited by 358 · see citing works
Importance of left atrial function in patients with myocardial infarction.
Matsuda, Y., Toma, Y., Ogawa, H., et al. (1983) · Circulation · doi:10.1161/01.cir.67.3.566 · Cited by 304 · see citing works
Myosin isoenzymes in normal and hypertrophied human ventricular myocardium.
Mercadier, J.-J., Bouveret, P., Gorza, L., Schiaffino, S., Clark, W. A., Zak, R., Bernard Swynghedauw, A., & Schwartz, K. (1983) · Circulation Research · doi:10.1161/01.res.53.1.52 · Cited by 279 · see citing works
The ATPase activities of rat cardiac myosin isoenzymes
Pope, B. J., Hoh, J. F. Y., & Weeds, A. G. (1980) · FEBS Letters · doi:10.1016/0014-5793(80)80219-5 · Cited by 259 · see citing works
Structural differences in the heavy chains of rat ventricular myosin isoenzymes
Jf, H., YEOH, G. P. S., Thomas, M. A., et al. (1979) · FEBS Letters · doi:10.1016/0014-5793(79)80115-5 · Cited by 225 · see citing works
Alteration of contractile function and excitation-contraction coupling in dilated cardiomyopathy.
Hasenfuss, G. P., Mulieri, L. A., Leavitt, B. J., Allen, P. D., Haeberle, J. R., & Alpert, N. R. (1992) · Circulation Research · doi:10.1161/01.res.70.6.1225 · Cited by 221 · see citing works
Holubarsch, C., Goulette, R., Litten, R. Z., Martin, B. J., Mulieri, L. A., & Alpert, N. R. (1985) · Circulation Research · doi:10.1161/01.res.56.1.78 · Cited by 208 · see citing works
Regulation of myosin heavy chain genes in the heart.
Morkin, E. (1993) · Circulation · doi:10.1161/01.cir.87.5.1451 · Cited by 199 · see citing works
Hasenfuss, G. P., Mulieri, L. A., Blanchard, E. M., Holubarsch, C., Leavitt, B. J., Ittleman, F. P., & Alpert, N. R. (1991) · Circulation Research · doi:10.1161/01.res.68.3.836 · Cited by 185 · see citing works
Reiser, P. J., & Kline, W. O. (1998) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.1998.274.3.h1048 · Cited by 156 · see citing works
Self-citationTakahashi, T., Schunkert, H., Isoyama, S., Wei, J. Y., Nadal‐Ginard, B., Grossman, W., & Izumo, S. (1992) · Journal of Clinical Investigation · doi:10.1172/jci115675 · Cited by 155 · see citing works
Hirzel, H. O., Tuchschmid, C. R., Schneider, J., Krayenbuehl, H. P., & SCHAUB, M. C. (1985) · Circulation Research · doi:10.1161/01.res.57.5.729 · Cited by 116 · see citing works
Wessels, A., Vermeulen, J. L. M., Virágh, S., Kálmán, F., Lamers, W. H., & Moorman, A. F. M. (1991) · The Anatomical Record · doi:10.1002/ar.1092290309 · Cited by 113 · see citing works
Fiber types and myosin types in human atrial and ventricular myocardium. An anatomical description.
Bouvagnet, P., Léger, J. J., Pons, F., et al. (1984) · Circulation Research · doi:10.1161/01.res.55.6.794 · Cited by 97 · see citing works
Functional significance of altered myosin adenosine triphosphatase activity in enlarged hearts
Alpert, N. R., Mulieri, L. A., & Litten, R. Z. (1979) · The American Journal of Cardiology · doi:10.1016/0002-9149(79)90227-3 · Cited by 92 · see citing works
Schier, J. J., & Adelstein, R. S. (1982) · Journal of Clinical Investigation · doi:10.1172/jci110521 · Cited by 87 · see citing works
Heat, mechanics, and myosin ATPase in normal and hypertrophied heart muscle.
Alpert, N. R., & Mulieri, L. A. (1982) · PubMed · Cited by 83 · see citing works
Matsuzaki, M., Tamitani, M., Toma, Y., et al. (1991) · The American Journal of Cardiology · doi:10.1016/0002-9149(91)90876-m · Cited by 82 · see citing works
Cummins, P., & Lambert, S. J. (1986) · Circulation Research · doi:10.1161/01.res.58.6.846 · Cited by 73 · see citing works
Left atrial mechanical and biochemical adaptation to pacing induced heart failure
Hoit, B. D., Shao, Y., Gabel, M., et al. (1995) · Cardiovascular Research · doi:10.1016/s0008-6363(96)88521-x · Cited by 63 · see citing works
Tsuchimochi, H., Kuro‐o, M., Takaku, F., et al. (1986) · Japanese Circulation Journal-english Edition · doi:10.1253/jcj.50.1044 · Cited by 18 · see citing works
Buttrick, P. M., Perla, C., Malhotra, A., et al. (1991) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.1991.260.2.h473 · Cited by 18 · see citing works
Hoffmann, U., & Siegert, E. (1987) · Basic Research in Cardiology · doi:10.1007/bf01907022 · Cited by 12 · see citing works
Myosin isoenzymes in normal and hypertrophied human hearts.
Hoffmann, U., Axmann, C., & Grisk, A. (1986) · PubMed · Cited by 9 · see citing works
Flagged first, then by citations
Cited by
Sorted by citations
Hypertrophic Cardiomyopathy: Genetics, Pathogenesis, Clinical Manifestations, Diagnosis, and Therapy
Marian, A. J., & Braunwald, E. (2017) · Circulation Research · doi:10.1161/circresaha.117.311059 · Cited by 1,403 · see citing works
Instrumented cardiac microphysiological devices via multimaterial three-dimensional printing
Lind, J. U., Busbee, T. A., Valentine, A. D., Pasqualini, F. S., Yuan, H., Yadid, M., Park, S.-J., Kotikian, A., Nesmith, A. P., Campbell, P. H., et al. (2017) · Nature Materials · doi:10.1038/nmat4782 · Cited by 863 · see citing works
Zhang, D., Shadrin, I. Y., Lam, J., Xian, H.-Q., Snodgrass, H. R., & Bursac, N. (2013) · Biomaterials · doi:10.1016/j.biomaterials.2013.04.026 · Cited by 565 · see citing works
Small and large animal models in cardiac contraction research: advantages and disadvantages
Milani-Nejad, N., & Janssen, P. M. L. (2014) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2013.10.007 · Cited by 484 · see citing works
Maturing human pluripotent stem cell-derived cardiomyocytes in human engineered cardiac tissues
Feric, N. T., & Radisic, M. (2016) · Advanced Drug Delivery Reviews · doi:10.1016/j.addr.2015.04.019 · Cited by 247 · see citing works
Cai, W., Zhang, J., de Lange, W. J., Gregorich, Z. R., Karp, H., Farrell, E. T., Mitchell, S. D., Tucholski, T., Lin, Z., Biermann, M., et al. (2019) · Circulation Research · doi:10.1161/circresaha.119.315305 · Cited by 78 · see citing works
James, J., Martin, L., Krenz, M., Quatman, C., Jones, F., Klevitsky, R., Gulick, J., & Robbins, J. (2005) · Circulation · doi:10.1161/01.cir.0000164233.09448.b1 · Cited by 77 · see citing works
ERRγ enhances cardiac maturation with T-tubule formation in human iPSC-derived cardiomyocytes
Miki, K., Deguchi, K., Nakanishi-Koakutsu, M., Lucena-Cacace, A., Kondo, S., Fujiwara, Y., Hatani, T., Sasaki, M., Naka, Y., Okubo, C., et al. (2021) · Nature Communications · doi:10.1038/s41467-021-23816-3 · Cited by 76 · see citing works
Human heart disease: lessons from human pluripotent stem cell-derived cardiomyocytes
Giacomelli, E., Mummery, C. L., & Bellin, M. (2017) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-017-2546-5 · Cited by 60 · see citing works
Fuller, G. A., Bicer, S., Hamlin, R. L., Yamaguchi, M., & Reiser, P. J. (2007) · Journal of Cardiac Failure · doi:10.1016/j.cardfail.2007.05.006 · Cited by 11 · see citing works
Self-citation
- Authors
- Reiser, P. J., Portman, M. A., Ning, X.-H., & Moravec, C. S.
- Affiliations
- The Ohio State University (US)
- University of Washington (US)
- Cleveland Clinic (US)
- Venue
- American Journal of Physiology-Heart and Circulatory Physiology
- Publisher
- American Physiological Society
- Published
- 2001-04-01
- Volume
- 280
- Issue
- 4
- Pages
- H1814-H1820
- ISSN
- 0363-6135 (ISSN-L)
- 1522-1539
- OpenAlex
- W2137542902
- Cited by
- 351
- References
- 31
- Citations by year
- 2026: 8 · 2025: 22 · 2024: 15 · 2023: 26 · 2022: 16 · 2021: 26 · 2020: 18 · 2019: 15 · 2018: 16 · 2017: 17 · 2016: 15 · 2015: 26 · 2014: 15 · 2013: 13 · 2012: 10
- FWCI
- 6.28
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Journal of Physiology-Heart and Circulatory Physiology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (1r29hl049929-01)
- National Heart, Lung, and Blood Institute (HL49929, R01HL060666)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (R24HD000836)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiomyopathy and Myosin Studies
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
- Keywords
- cardiac myosin heavy chain, myosin isoforms, heart failure, fetal heart development, atrium, ventricles, dilated cardiomyopathy, ischemic cardiomyopathy, human myocardium
- MeSH terms
- Adolescent, Adult, Aged, Cardiomyopathy, Dilated, Female, Embryonic and Fetal Development, Fetal Heart, Fetus, Gestational Age, Heart Atria, Heart Ventricles, Humans, Male, Middle Aged, Myocardium, Myocardial Ischemia, Myosin Heavy Chains, Protein Isoforms
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
