ArticleCirculation research2015
GDF11 does not rescue aging-related pathological hypertrophy.
Article in Circulation research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 119 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
119 citing papers in PubMed, 185 citations in OpenAlex.
- Infusion of young donor plasma components in older patients modifies the immune and inflammatory response to surgical tissue injury: a randomized clinical trial.Journal of translational medicine · 2025Trial
- Age Trends in Growth and Differentiation Factor-11 and Myostatin Levels in Healthy Men, and Differential Response to Testosterone, Measured Using Liquid Chromatography-Tandem Mass Spectrometry.The journals of gerontology. Series A, Biological sciences and medical sciences · 2022Trial
- Non-Coding RNAs from Cardiac Development to Disease: Regulatory Context, Regenerative Potential, and Translational Limits.International journal of molecular sciences · 2026Review
- Elevated circulating GDF11 and its role in age-related sarcopenia: insights from clinical, transcriptomic, andFrontiers in aging · 2026Article
- GDF11-secreting cell transplant efficiently ameliorates age-related pulmonary fibrosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Review
- Activated GDF11/8 subforms predict cardiovascular events and mortality in humans.Nature communications · 2025Article
- GDF11 Regulates M1 and M2 Polarization of BV2 Microglial Cells via p38 MAPK Signaling Pathway.Molecular neurobiology · 2025Article
- Geroscience in heart failure: the search for therapeutic targets in the shared pathobiology of human aging and heart failure.The journal of cardiovascular aging · 2025Article
- Reducing functionally defective old HSCs alleviates aging-related phenotypes in old recipient mice.Cell research · 2025Article
- Novel insights into the pleiotropic health effects of growth differentiation factor 11 gained from genome-wide association studies in population biobanks.BMC genomics · 2024Article
- Aging insights from heterochronic parabiosis models.npj aging · 2024Review
- Rejuvenation of young blood on aging organs: Effects, circulating factors, and mechanisms.Heliyon · 2024Review
- Blood-based therapies to combat neurodegenerative diseases.Metabolic brain disease · 2024Review
- Circulating Growth Differentiation Factors 11 and 8, Their Antagonists Follistatin and Follistatin-Like-3, and Risk of Heart Failure in Elders.The journals of gerontology. Series A, Biological sciences and medical sciences · 2024Article
- Circulating GDF11 exacerbates myocardial injury in mice and associates with increased infarct size in humans.Cardiovascular research · 2023Article
- Disorganization of secondary lymphoid organs and dyscoordination of chemokine secretion as key contributors to immune aging.Seminars in immunology · 2023Review
- Evaluation of Associations of Growth Differentiation Factor-11, Growth Differentiation Factor-8, and Their Binding Proteins Follistatin and Follistatin-Like Protein-3 With Dementia and Cognition.The journals of gerontology. Series A, Biological sciences and medical sciences · 2023Article
- GDF11 and aging biology - controversies resolved and pending.The journal of cardiovascular aging · 2023Article
- Targeting aging with the healthy skeletal system: The endocrine role of bone.Reviews in endocrine & metabolic disorders · 2023Review
59 more citing papers are in PubMed but not listed here.
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Authors and funding
19 authors at 1 institution in 1 country.
Funding
Abstract
rationaleGrowth differentiation factor 11 (GDF11) is a member of the transforming growth factor-β super family of secreted factors. A recent study showed that reduced GDF11 blood levels with aging was associated with pathological cardiac hypertrophy (PCH) and restoring GDF11 to normal levels in old mice rescued PCH.
objectiveTo determine whether and by what mechanism GDF11 rescues aging dependent PCH. METHODS AND
resultsTwenty-four-month-old C57BL/6 mice were given a daily injection of either recombinant (r) GDF11 at 0.1 mg/kg or vehicle for 28 days. rGDF11 bioactivity was confirmed in vitro. After treatment, rGDF11 levels were significantly increased, but there was no significant effect on either heart weight or body weight. Heart weight/body weight ratios of old mice were not different from 8- or 12-week-old animals, and the PCH marker atrial natriuretic peptide was not different in young versus old mice. Ejection fraction, internal ventricular dimension, and septal wall thickness were not significantly different between rGDF11 and vehicle-treated animals at baseline and remained unchanged at 1, 2, and 4 weeks of treatment. There was no difference in myocyte cross-sectional area rGDF11 versus vehicle-treated old animals. In vitro studies using phenylephrine-treated neonatal rat ventricular myocytes, to explore the putative antihypertrophic effects of GDF11, showed that GDF11 did not reduce neonatal rat ventricular myocytes hypertrophy, but instead induced hypertrophy.
conclusionsOur studies show that there is no age-related PCH in disease-free 24-month-old C57BL/6 mice and that restoring GDF11 in old mice has no effect on cardiac structure or function.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.