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Growth Differentiation Factor 11 Is a Circulating Factor that Reverses Age-Related Cardiac Hypertrophy
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The most common form of heart failure occurs with normal systolic function and often involves cardiac hypertrophy in the elderly. To clarify the biological mechanisms that drive cardiac hypertrophy in aging, we tested the influence of circulating factors using heterochronic parabiosis, a surgical technique in which joining of animals of different ages leads to a shared circulation. After 4 weeks of exposure to the circulation of young mice, cardiac hypertrophy in old mice dramatically regressed, accompanied by reduced cardiomyocyte size and molecular remodeling. Reversal of age-related hypertrophy was not attributable to hemodynamic or behavioral effects of parabiosis, implicating a blood-borne factor. Using modified aptamer-based proteomics, we identified the TGF-β superfamily member GDF11 as a circulating factor in young mice that declines with age. Treatment of old mice to restore GDF11 to youthful levels recapitulated the effects of parabiosis and reversed age-related hypertrophy, revealing a therapeutic opportunity for cardiac aging.
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“the rejuvenation strategies based on the use of blood-borne systemic factors identified in parabiosis experiments (Conboy et al., 2005; Loffredo et al., 2013; Villeda et al., 2011).”
From The Hallmarks of Aging (2013) · cites this paper as Loffredo et al., 2013
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“Excitingly, proof of principle exists for rejuvenation through blood-borne systemic factors (Conboy et al., 2005; Loffredo et al., 2013; Villeda et al., 2011).”
From The Hallmarks of Aging (2013) · cites this paper as Loffredo et al., 2013
In the citing paper
“The first study42 focused on the monomeric forms of GDF11 and myostatin and showed that they cumulatively decrease in abundance in serum with aging42,44.”
From The central role of muscle stem cells in regenerative failure with aging (2015) · cites this paper as [44]
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“Intriguingly, at least part of the ‘rejuvenating’ effect of a young systemic environment appears related to the higher levels of circulating growth differentiation factor 11 (GDF11) and oxytocin present in young blood as compared to aged38,166,168,169.”
From Stem cell aging: mechanisms, regulators and therapeutic opportunities (2014) · cites this paper as [168]
In the citing paper
“Studies on heterochronic parabiosis and plasma exchange in animals have demonstrated that circulating proteins can have a causal influence on ageing phenotypes across the body, including in skeletal muscle107,108, heart109 and brain15,110–112.”
From Measuring biological age using omics data (2022) · cites this paper as [109]
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“이로부 터 늙은 생쥐의 혈액 속에 있는 wingless-type MMTV integration site family, member 3a [92], transforming growth factor beta 1 [93], C-C motif chemokine ligand 11 [94], β2-microglobulin [95] 등이 노화촉진인자로, 젊은 생쥐의 혈액 속에 있는 growth differentiation factor 11 (GDF11)이 노화억제 인자, 즉 회춘인자로 확인되었다[96].”
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Jin, M., Cao, R., Niu, X., & Shan, P. (2023) · Archives of Osteoporosis · doi:10.1007/s11657-023-01237-7
“Our results were also consistent with reported by an in vivo study performed by Loffredo et al., who first identified GDF11 (a member of the TGF-β super-family) as a circulating factor in young mice and reported an age-related decline in this factor [16].”
InfluentialParabiosis reinvigorates age-related bone quality through Wnt/β-catenin signalingPreprint
Feng, R., Yu, T., Duan, X., Wu, G., Huang, Y., & Hu, H. (2023) · Research Square · doi:10.21203/rs.3.rs-2961382/v1
Лунева, С. Н., Ивановна, М. Т., Майоровна, А. А., Выхованец, Е. П., & Matveeva, K. P. (2023) · Pediatric Traumatology Orthopaedics and Reconstructive Surgery · doi:10.17816/ptors529677
Unlocking the dark matter: noncoding RNAs and RNA modifications in cardiac aging
Kang, J., Rhee, J., Wang, C., Yang, Y., Li, G., & Li, H. (2024) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00532.2023
GDF11 level and its effect on prognosis in patients with acute myeloid leukemia
Aslan, N. A., Avcı, E., Şenol, H., & Güler, N. (2024) · Journal of Investigative Medicine · doi:10.1177/10815589241238218
Squires, E. J. (2024) · CABI eBooks · doi:10.1079/9781800620742.0002
Ophthalmic acid is a bloodborne metabolite that contributes to age-induced cardiomyocyte hypertrophyPreprint
Mehdipour, M., Park, S., Wei, W., Long, J. Z., & Huang, G. N. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.08.08.607218
“Though these markers may be indicative of cardiac hypertrophy to an extent, we did not observe differential expression of these genes in relation to age, and this was apparent in the study reported by Loffredo et al 4 .”
BackgroundMethodResultInfluentialLee, W. W.-H., Lee, D. W.-C., & Lee, A. Y. (2024) · Current Treatment Options in Cardiovascular Medicine · doi:10.1007/s11936-024-01054-2
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Potential Molecular Mechanism of FNDC4 Protection Against Aging in the Heart
Matsushita, M., & Sadoshima, J. (2025) · JACC Basic to Translational Science · doi:10.1016/j.jacbts.2025.04.018
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Yu, C., Xiaomao, T., Luo, J., Wan, Y., Hong, Y., Liu, Z., Zhang, J., Pei, J., He, X., Wen, S., et al. (2025) · PLoS ONE · doi:10.1371/journal.pone.0331020 · Cited by 1
“It also reversed myelin regeneration in aged rats [12], promoted neurogenesis, improved cognitive function [13], and even reversed myocardial hypertrophy in aged rats [14].”
GDF11 and its receptor ALK4 independently modulate human myoblast migration and fusionPreprint
Reis, R. F., da Silva, I. F., Costa-Santos, B. G., Bagri, K. M., Costa, M. L., Mouly, V., Savino, W., Cotta-de-Almeida, V., Mermelstein, C., Jurberg, A. D., et al. (2025) · Research Square · doi:10.21203/rs.3.rs-7777108/v1
Metadata
- Authors
- Loffredo, F. S., Steinhauser, M. L., Jay, S. M., Gannon, J., Pancoast, J. R., Yalamanchi, P., Sinha, M., Dall’Osso, C., Khong, D., Shadrach, J. L., Miller, C. M., Singer, B. S., Stewart, A., Psychogios, N., Gerszten, R. E., Hartigan, A. J., Kim, M.-J., Serwold, T., Wagers, A. J., & Lee, R. T.
- Affiliations
- Brigham and Women's Hospital (US)
- SomaLogic (United States) (US)
- Massachusetts General Hospital (US)
- Corresponding author
- Wagers, Amy J.
- Lee, Richard T.
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2013-05
- Volume
- 153
- Issue
- 4
- Pages
- 828-839
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC3677132
- OpenAlex
- W2156589853
- Cited by
- 948
- References
- 64
- Citations by year
- 2026: 44 · 2025: 46 · 2024: 53 · 2023: 67 · 2022: 69 · 2021: 69 · 2020: 87 · 2019: 70 · 2018: 86 · 2017: 91 · 2016: 94 · 2015: 84 · 2014: 56 · 2013: 30
- FWCI
- 59.87
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Digital Access to Scholarship at Harvard (DASH) (Harvard University) (submittedVersion, cc-by)
- Archivio Istituzionale della Ricerca - Università degli Studi della Campania "Luigi Vanvitelli" (submittedVersion)
- Funders
- Howard Hughes Medical Institute
- American Heart Association
- National Institutes of Health (1dp2od004345-01)
- Harvard Stem Cell Institute
- National Institute on Aging (R01AG033053, R01AG032977, R01AG040019)
- National Heart, Lung, and Blood Institute (U01HL100402, K99HL112905, R00HL112905)
- National Institute of Diabetes and Digestive and Kidney Diseases (K08DK090147, P30DK036836)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Congenital heart defects research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
- Keywords
- GDF11, cardiac hypertrophy, cardiac aging, heterochronic parabiosis, circulating factors, heart failure with preserved ejection fraction, cardiomyocyte size, TGF-beta superfamily, aptamer-based proteomics, regenerative therapy
- MeSH terms
- Aging, Animals, Blood Pressure, Female, Cardiomegaly, Humans, Male, Mice, Inbred C57BL, Parabiosis, Hypertrophy, Left Ventricular, Bone Morphogenetic Proteins, Myocytes, Cardiac, Mice, Forkhead Transcription Factors, Growth Differentiation Factors, Induced Pluripotent Stem Cells
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