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Growth Differentiation Factor 11 Is a Circulating Factor that Reverses Age-Related Cardiac Hypertrophy
Open accessAbstract
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]
In the citing paper
“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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Stem Cells as Vehicles for Youthful Regeneration of Aged Tissues
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“Circulating factors that came from young mice ameliorated muscleregeneration(5),neurodegeneration(6),andcardiac hypertrophy (7) in agedmice.”
BackgroundSystemic milieu and age-related deterioration
Zhang, H., Cherian, R., & Jin, K. (2019) · GeroScience · doi:10.1007/s11357-019-00075-1 · Cited by 35
GDF11 Antagonizes Psoriasis-like Skin Inflammation via Suppression of NF-κB Signaling Pathway
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“A reduction in serum GDF11 levels is associated with age-related cardiac hypertrophy [16].”
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“By proteomics studies, growth differentiation factor 11 (GDF11), a member of the activin/TGF-b superfamily, was identified as a factor that carries the potential to reverse cardiac hypertrophy.(146) Recent publications,(147,148) however, have raised questions about the age-dependent reduction of GDF11 and its antihype…”
BackgroundSelf-citationThe vasculature as a neural stem cell niche
Otsuki, L., & Brand, A. H. (2017) · Neurobiology of Disease · doi:10.1016/j.nbd.2017.01.010 · Cited by 34
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GDF11 Modulates Ca2+-Dependent Smad2/3 Signaling to Prevent Cardiomyocyte Hypertrophy
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“The data presented here are consistent with other reports describing the antihypertrophic effects of GDF11 both in vivo and in vitro [6,20].”
BackgroundResultInfluentialSystemic Blockade of ACVR2B Ligands Protects Myocardium from Acute Ischemia-Reperfusion Injury
Magga, J. M., Vainio, L., Kilpiö, T., Hulmi, J. J., Taponen, S., Lin, R., Ramste, M. O., Szabó, Z., Gao, E., Rahtu‐Korpela, L., et al. (2019) · Molecular Therapy · doi:10.1016/j.ymthe.2019.01.013 · Cited by 32
“GDF11 was formerly considered as a rejuvenation factor, and restoration of levels of GDF11 were shown to provide protection from age-related pathological cardiac hypertrophy.(45) In subsequent studies, aging was not associated with a decrease in circulating GDF11 levels,(46) and elevation of GDF11 did not provide ther…”
BackgroundGDF11 Implications in Cancer Biology and Metabolism. Facts and Controversies
Nieves, A. S., Gerardo‐Ramírez, M., Pedraza-Vázquez, G., Chávez-Rodríguez, L., Bucio, L., Souza, V., Miranda-Labra, R. U., Gómez-Quiroz, L. E., & Gutiérrez‐Ruíz, M. C. (2019) · Frontiers in Oncology · doi:10.3389/fonc.2019.01039 · Cited by 37
“GDF11 shares 89% amino acid sequence homology with GDF8, however GDF8 expression in human tissues is restricted to cardiac and skeletal muscle (1), while GDF11 is practically expressed in all tissues (15).”
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“To clarify the role of GDF11 in aging cartilage, we first proved that the level of GDF11 was reduced with age in the circulation in humans and mice, and its levels were restored by heterochronic parabiosis (Figure 2), which is consistent with previous results (4,6,13).”
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“[52] suggested that GDF11 could be responsible for these effects.”
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The systemic milieu as a mediator of dietary influence on stem cell function during ageing
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“Notably, GDF11 also comprises a circulating factor in blood [41].”
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“For example, GDF11 has been reported to inhibit myocardial hypertrophy and decrease with age [59].”
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“GDF11, another member of the TGF-β superfamily, was recently identified as a regenerative factor that ameliorates age-related cardiac hypertrophy [40], slows vascular deterioration, and promotes brain neurogenesis [41] and skeletal muscle repair [42].”
Aging Systemic Milieu Impairs Outcome after Ischemic Stroke in Rats
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“Agerelated cardiac hypertrophy can also be reversed by exposure to a young systemic milieu, accompanied by reduced cardiomyocyte size and molecular remodeling [3].”
BackgroundTMT‐Based Quantitative Proteomic Analysis Reveals Proteomic Changes Involved in Longevity
Wang, Z., Zhang, R., Liu, F., Jiang, P., Xu, J., Cao, H., Du, X., Ma, L., Lin, F., Cheng, L. Y., et al. (2018) · PROTEOMICS - CLINICAL APPLICATIONS · doi:10.1002/prca.201800024 · Cited by 30
Growth differentiation factor 11 (GDF11) has pronounced effects on skin biology
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“We demonstrated that GDF11 levels decrease with age, which aligns with original reports by Loffredo and colleagues (1) and a recent study by Poggioli and colleagues (8).”
BackgroundResultOpstad, T. B., Kalstad, A. A., Pettersen, A. R., Arnesen, H., & Seljeflot, I. (2019) · Experimental Gerontology · doi:10.1016/j.exger.2019.01.020 · Cited by 32
“In parabiosis experiments, it was demonstrated that older mice sharing blood supply with younger developed a younger phenotype with improved olfaction, regression of myocardial injury and better memory, and it was suggested that GDF11 was the rejuvenating factor causal for these alterations (Loffredo et al., 2013; Kat…”
BackgroundCrystal structure of human GDF11
Padyana, A. K., Vaidialingam, B., Hayes, D., Gupta, P., Franti, M., & Farrow, N. A. (2016) · Acta Crystallographica Section F Structural Biology Communications · doi:10.1107/s2053230x16001588 · Cited by 29
“The biological role of growth differentiation factor 11 (GDF11) has recently been the focus of intense debate (Brun & Rudnicki, 2015; Egerman et al., 2015; Katsimpardi et al., 2014; Leinwand & Harrison, 2013; Loffredo et al., 2013; Poggioli et al., 2016; Sinha et al., 2014; Smith et al., 2015).”
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“proceeded to identify GDF11 as a circulating factor that declined with age and could reverse cardiac hypertrophy when injected into older animals (7).”
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Patel, V. K., & Demontis, F. (2014) · Aging · doi:10.18632/aging.100666 · Cited by 30
Aging as a loss of morphostatic information: A developmental bioelectricity perspective
Pio‐Lopez, L., & Levin, M. G. (2024) · Ageing Research Reviews · doi:10.1016/j.arr.2024.102310 · Cited by 36
Proteomics: Clinical and research applications in respiratory diseases
Norman, K. C., Moore, B. B., Arnold, K. B., & O’Dwyer, D. N. (2018) · Respirology · doi:10.1111/resp.13383 · Cited by 29
Bai, X. (2018) · Advances in experimental medicine and biology · doi:10.1007/978-981-13-1117-8_14 · Cited by 32
Mixing old and young: enhancing rejuvenation and accelerating aging
Lau, A., Kennedy, B. K., Kirkland, J. L., & Tullius, S. G. (2019) · Journal of Clinical Investigation · doi:10.1172/jci123946 · Cited by 29
“Initially identified in a proteomic screen of factors that were more prevalent in sera of young mice relative to those of old mice (13), GDF11 was shown to reduce cardiac hypertrophy and age-associated defects in muscle regeneration (13, 17).”
BackgroundConsidering Cause and Effect of Immune Cell Aging on Cardiac Repair after Myocardial Infarction
Tobin, S. W., Alibhai, F. J., Weisel, R. D., & Li, R. (2020) · Cells · doi:10.3390/cells9081894 · Cited by 30
Jiao, L., Shao, Y., Yu, Q., Li, M., Wang, Y., Gong, M., Yang, X., Liu, T., Li, Z., Liu, H., et al. (2020) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2020.173495 · Cited by 30
Promoting healthy cardiovascular aging: emerging topics
Clayton, Z. S., Craighead, D. H., Darvish, S., Coppock, M. E., Ludwig, K. R., Brunt, V. E., Seals, D. R., & Rossman, M. J. (2022) · The Journal of Cardiovascular Aging · doi:10.20517/jca.2022.27 · Cited by 29
Living long and ageing well: is epigenomics the missing link between nature and nurture?
The ACUME2 Project, Rea, I. M., Dellett, M., & Mills, K. (2015) · Biogerontology · doi:10.1007/s10522-015-9589-5 · Cited by 29
“…that the newly described growth differentiation factor (GDF11) could act as a potential reversal agent for sarcopenia and ageing seems to have been muted by recent research, apparently contradicting the original effects of GDF11 (Egerman et al. 2015; Sinha et al. 2014; Loffredo et al. 2013).”
ResultThe Growth Differentiation Factor 11 (GDF11) and Myostatin (MSTN) in tissue specific aging
Fan, X., Gaur, U., Sun, L., Yang, D., & Yang, M. (2017) · Mechanisms of Ageing and Development · doi:10.1016/j.mad.2017.04.009 · Cited by 30
“However, if the GDF11 levels are restored to normal, it can rescue the PCH in aged mice (Loffredo et al., 2013).”
Gulej, R., Patai, R., Ungvari, A., Kállai, A., Tarantini, S., Yabluchanskiy, A., Huffman, D. M., Conboy, M. J., Conboy, I. M., Mika Kivimaki, B., et al. (2025) · GeroScience · doi:10.1007/s11357-025-01657-y · Cited by 29
Castellano, J. M., Palner, M., Li, S., Freeman, G. M., Nguyen, A., Shen, B., Stan, T. M., Mosher, K. I., Chin, F. T., de Lecea, L., et al. (2016) · Scientific Reports · doi:10.1038/srep29015 · Cited by 29
Wang, L., Wang, Y., Wang, Z., Qi, Y., Zong, B., Liu, M., Li, X., Zhang, X., Liu, C., Cao, R., et al. (2018) · American Journal of Physiology-Gastrointestinal and Liver Physiology · doi:10.1152/ajpgi.00159.2018 · Cited by 29
“Previous studies have shown that restoring systemic GDF11 level reversed age-related cardiac hypertrophy and brain dysfunction (20, 23).”
BackgroundThe Effects of Parabiosis on Aging and Age-Related Diseases
Ashapkin, V. V., Kutueva, L. I., & Vanyushin, B. F. (2020) · Advances in experimental medicine and biology · doi:10.1007/978-3-030-42667-5_5 · Cited by 28
Yang, J., Kong, C., Jia, L., Li, T., Quan, M., Li, Y., Lyu, D., Li, F., Jin, H., Li, Y., et al. (2021) · Alzheimer s Research & Therapy · doi:10.1186/s13195-021-00845-0 · Cited by 29
“Specifically, some studies have suggested that reduced GDF11 blood levels are responsible for age-related cardiac hypertrophy [33] and skeletal muscle dysfunction [34], while others have shown that increasing levels of GDF11 can induce skeletal and cardiac muscle wasting [35, 36].”
BackgroundChen, L., Luo, G., Liu, Y., Lin, H., Zheng, C., Xie, D., Zhu, Y., Chen, L., Huang, X., Hu, D., et al. (2021) · Cell Death and Disease · doi:10.1038/s41419-021-03954-8 · Cited by 28
Growth differentiation factor 11 accelerates liver senescence through the inhibition of autophagy
Sun, J. M., Li, Y., Yang, X. F., Dong, W., Yang, J., Hu, Q. Z., Zhang, C., Fang, H., & Liu, A. (2021) · Aging Cell · doi:10.1111/acel.13532 · Cited by 27
“…factor (GDF) 11, one of the factors identified in systemic milieu, has been shown to reduce age- related cardiac hypertrophy of the heart (Loffredo et al., 2013; Poggioli et al., 2016), skeletal muscle and stem cell dysfunction (Sinha et al., 2014), and decline in neurogenesis and…”
BackgroundSingle-cell transcriptomics of peripheral blood in the aging mouse
Teo, Y. V., Hinthorn, S. J., Webb, A. E., & Neretti, N. (2023) · Aging · doi:10.18632/aging.204471 · Cited by 28
“Parabiosis of young and old mice has been shown to reverse cardiac hypertrophy in old mouse and rejuvenate aged satellite cells (12, 13).”
Kraler, S. C., Balbi, C., Vdovenko, D., Lapikova-Bryhinska, T., Camici, G. G., Liberale, L., Bonetti, N. R., Díaz-Cañestro, C., Burger, F., Roth, A., et al. (2023) · Cardiovascular Research · doi:10.1093/cvr/cvad153 · Cited by 28
“…GDF11 on cardiac structure intertwined with the consistently observed I/R-and age-dependent decline in myocardial Gdf11 across independent studies, 27,57–60 we next sought to study the cardiac effects of boosting endogenous GDF11 by rGDF11 delivery prior to I/R injury in both young (3–4 months)…”
BackgroundMethodInfluentialEpidemiology of donors and recipients: lessons from the SCANDAT database
Edgren, G., & Hjalgrim, H. (2017) · Transfusion Medicine · doi:10.1111/tme.12487 · Cited by 29
“…research, which has been triggered by a series of animal model studies, has indicated a wide range of beneficial health effects, including improved cognitive function (Katsimpardi et al., 2014; Villeda et al., 2014), muscle strength (Sinha et al., 2014) and cardiac function (Loffredo et al., 2013).”
BackgroundGDF11/BMP11 as a novel tumor marker for liver cancer
Zhang, Y., Pan, L., Pang, Y., Yang, J., Lv, M., Liu, F., Qu, X., Chen, X., Gong, H., Liu, D., et al. (2018) · Experimental and Therapeutic Medicine · doi:10.3892/etm.2018.5861 · Cited by 28
“…upregulation of p-Smad3 in multiple cell types, including pluripotent stem cell-derived cardiomyocytes, human skeletal muscle-derived cells and human umbilical vein endothelial cells, to regulate cell proliferation and muscle regeneration (10,13,14,30), which is consistent with the present results.”
Sadlowski, C. M., Balderston, S., Sandhu, M., Hajian, R., Liu, C., Tran, T. P., Conboy, M. J., Paredes, J., Murthy, N., Conboy, I. M., et al. (2018) · Lab on a Chip · doi:10.1039/c8lc00446c · Cited by 28
Circulating GDF11 levels are decreased with age but are unchanged with obesity and type 2 diabetes
Añón-Hidalgo, J., Catalán, V., Rodrı́guez, A., Ramírez, B., Silva, C., Galofré, J. C., Salvador, J., Frühbeck, G., & Gómez‐Ambrosi, J. (2019) · Aging · doi:10.18632/aging.101865 · Cited by 28
“GDF11 has been reported to exert anti-aging effects promoting skeletal muscle [15], heart [16] and brain [17] regeneration in mice.”
BackgroundRejuvenation: It’s in Our Blood
Bitto, A., & Kaeberlein, M. R. (2014) · Cell Metabolism · doi:10.1016/j.cmet.2014.06.007 · Cited by 27
“GDF11, a member of the TGF-b superfamily, declines in blood with age (Loffredo et al., 2013), and restoration of youthful levels of GDF11 are sufficient to Heterochronic parabiosis, in which a young mouse and an aged mouse share circulatory systems, improves the health of the aged mouse while…”
BackgroundAged Mice Repeatedly Injected with Plasma from Young Mice: A Survival Study
Shytikov, D. W., Balva, O., Debonneuil, É., Glukhovskiy, P., & Pishel, I. (2014) · BioResearch open access · doi:10.1089/biores.2014.0043 · Cited by 26
“Indeed, age-related changes in the immune system play important roles in pathogenesis of many disorders associated with age.(22) It is well known that T cells are one of the most affected units during aging, and age-related changes in T cells have been amply documented, with an increase in the number of CD8 + cells an…”
BackgroundYoung plasma attenuates age‐dependent liver ischemia reperfusion injury
Liu, A., Yang, J., Hu, Q. Z., Dirsch, O., Dahmen, U., Zhang, C., Gewirtz, D. A., Fang, H., & Sun, J. (2018) · The FASEB Journal · doi:10.1096/fj.201801234r · Cited by 27
“Several recent studies show that infusion of blood obtained from young mice into old mice has therapeutic effect on aging-associated deterioration of organs, includingmuscle (5, 6), brain (7, 8), spinal cord (9), heart (10), and pancreas (11).”
BackgroundCandidate rejuvenating factor GDF11 and tissue fibrosis: friend or foe?
Frohlich, J., & Vinciguerra, M. (2020) · GeroScience · doi:10.1007/s11357-020-00279-w · Cited by 28
UNC5B Promotes Vascular Endothelial Cell Senescence via the ROS‐Mediated P53 Pathway
Yang, Z. L., Li, H., Luo, P., Yan, D., Yang, N., Zhang, Y., Huang, Y., Liu, Y., Zhang, L., Yan, J., et al. (2021) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2021/5546711 · Cited by 27
Laviano, A. (2014) · New England Journal of Medicine · doi:10.1056/nejmcibr1407158 · Cited by 27
Respiratory Mucosal Proteome Quantification in Human Influenza Infections
Marion, T. N., Elbahesh, H., Thomas, P. G., DeVincenzo, J. P., Webby, R. J., & Schughart, K. (2016) · PLoS ONE · doi:10.1371/journal.pone.0153674 · Cited by 27
“SOMAscan is highly sensitive with a threshold of detection of 30 femtomolar,<1 pg/ml and 10(8)-fold dynamic range for quantification of proteome changes in mice [25] and humans [22, 24, 26, 27].”
BackgroundGeroscience approaches to increase healthspan and slow aging
Melov, S. (2016) · F1000Research · doi:10.12688/f1000research.7583.1 · Cited by 27
Impaired regeneration in aged nerves: Clearing out the old to make way for the new
Scheib, J. L., & Höke, A. (2016) · Experimental Neurology · doi:10.1016/j.expneurol.2016.07.010 · Cited by 27
Liu, A., Dong, W., Peng, J., Dirsch, O., Dahmen, U., Fang, H., Zhang, C., & Sun, J. M. (2018) · The FASEB Journal · doi:10.1096/fj.201800195r · Cited by 27
Curley, M. K., Milne, L., Smith, S. E., J⊘rgensen, A., Frederiksen, H. W., Hadoke, P. W. F., Potter, P. K., & Smith, L. B. (2018) · The FASEB Journal · doi:10.1096/fj.201800612r · Cited by 28
Zhang, H., & Jin, K. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21061908 · Cited by 27
Tyshkovskiy, A., Kholdina, D., Ying, K., Davitadze, M., Molière, A., Tongu, Y., Kasahara, T., Kats, L., Vladimirova, A., Moldakozhayev, A., et al. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.07.04.601982 · Cited by 32
Rejuvenating Strategies of Tissue-specific Stem Cells for Healthy Aging
Wang, M., Chen, J., Chen, F., Liu, Q., Sun, Y., Chen, Y., Yang, T., Bao, Y., & Hu, Y. (2018) · Aging and Disease · doi:10.14336/ad.2018.1119 · Cited by 27
Parabiosis modeling: protocol, application and perspectives
Yang, C., 成都610072，中国, 中., Liu, Z., Wang, J., Bu, X., Wang, Y., Xiang, Y., 成都610072，中国, 中., 610083，中国, 西. 成., 陆军军医大学大坪医院神经内科和临床神经科学中心，重庆400012，中国, et al. (2021) · 动物学研究 · doi:10.24272/j.issn.2095-8137.2020.368 · Cited by 26
“Several studies also identified growth differentiation factor (GDF)-11 as a circulating rejuvenating factor (Katsimpardi et al., 2014; Loffredo et al., 2013; Sinha et al., 2014).”
Cardio- and Neurometabolic Adipobiology: Consequences and Implications for Therapy
Fröhlich, J., Chaldakov, G. N., & Vinciguerra, M. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22084137 · Cited by 31
“In 2013, GDF11 had been rediscovered and marked as a blood circulating “rejuvenating” cytokine that decreased with age and had the ability to reverse age-related phenotypes in old mice during heterochronic parabiosis experiments [57].”
BackgroundMyofiber Baf60c controls muscle regeneration by modulating Dkk3-mediated paracrine signaling
Xu, J., Li, X., Chen, W., Zhang, Z., Zhou, Y., Gou, Y., Lv, C.-A., Lu, J., Qiu, X., Ma, S., et al. (2023) · The Journal of Experimental Medicine · doi:10.1084/jem.20221123 · Cited by 26
“…has gained more attention in the last decade due to numerous reports demonstrating its functions in multiple systems, such as skeletal muscle, cardiac myocyte, and bone homeostasis, with inconsistent or even controversial results (Harper et al., 2016; Loffredo et al., 2013; Walker et al., 2016).”
Bukovský, A. (2015) · Reproductive Biology and Endocrinology · doi:10.1186/s12958-015-0001-8 · Cited by 26
“As indicated above, there is a recent boom dealing with the blood plasma involvement in rejuvenation of aging tissues [53-66].”
Background
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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