|
Cachexia
|
0.040 |
GeneticVariation
|
phenotype |
BEFREE |
Although GDF11 treatment can reduce pathological cardiac hypertrophy and associated fibrosis while improving cardiac pump function in pressure overload, high doses of GDF11 cause severe cachexia and death.
|
30571461 |
2018 |
|
Heart failure
|
0.020 |
GeneticVariation
|
disease |
BEFREE |
Recently, targeted myocardial delivery of the GDF11 gene in aged mice was found to reduce heart failure and enhance the proliferation of cardiac progenitor cells after myocardial ischemia-reperfusion (I-R).
|
30900023 |
2019 |
|
Congestive heart failure
|
0.020 |
GeneticVariation
|
disease |
BEFREE |
Recently, targeted myocardial delivery of the GDF11 gene in aged mice was found to reduce heart failure and enhance the proliferation of cardiac progenitor cells after myocardial ischemia-reperfusion (I-R).
|
30900023 |
2019 |
|
MYELODYSPLASTIC SYNDROME
|
0.020 |
GeneticVariation
|
group |
BEFREE |
Luspatercept (and sotatercept), ligand traps that particularly inhibit GDF11, lead to RBC transfusion independence in 10% to 50% of lower-risk MDSs resistant to available treatments, and have started to be used in PMF.
|
30602619 |
2019 |
|
Agenesis
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
We show that GDF11 is cleaved and activated by PCSK5A, but not by PCSK5A-C470R, and that Gdf11-deficient embryos, in addition to having anteroposterior patterning defects and renal and palatal agenesis, also have a presacral mass, anorectal malformation, and exomphalos.
|
18519639 |
2008 |
|
Primary Myelofibrosis
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
Luspatercept (and sotatercept), ligand traps that particularly inhibit GDF11, lead to RBC transfusion independence in 10% to 50% of lower-risk MDSs resistant to available treatments, and have started to be used in PMF.
|
30602619 |
2019 |
|
congenital lobulation of kidney
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
A variant in GDF11 (encoding growth differentiation factor 11), predicting a p.(Arg298Gln) substitution at the Furin protease cleavage site, was identified in one family that segregated with CL/P and both rib and vertebral hypersegmentation, mirroring that seen in Gdf11 knockout mice.
|
31215115 |
2019 |
|
Congenital omphalocele
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
We show that GDF11 is cleaved and activated by PCSK5A, but not by PCSK5A-C470R, and that Gdf11-deficient embryos, in addition to having anteroposterior patterning defects and renal and palatal agenesis, also have a presacral mass, anorectal malformation, and exomphalos.
|
18519639 |
2008 |
|
Congenital exomphalos
|
0.010 |
GeneticVariation
|
disease |
BEFREE |
We show that GDF11 is cleaved and activated by PCSK5A, but not by PCSK5A-C470R, and that Gdf11-deficient embryos, in addition to having anteroposterior patterning defects and renal and palatal agenesis, also have a presacral mass, anorectal malformation, and exomphalos.
|
18519639 |
2008 |
|
Neoplasms
|
0.060 |
Biomarker
|
group |
BEFREE |
In conclusion, GDF11 has a tumor suppressor role in liver cancer, exerts its effects through Smad2/3 signaling and may serve as a novel tumor marker in liver cancer diagnosis.
|
29545874 |
2018 |
|
Neoplasms
|
0.060 |
Biomarker
|
group |
BEFREE |
Intracellular GDF11 retention adds to the concept of tumor-suppressor inactivation and reveals a cell-biological vulnerability for TNBCs lacking therapeutically actionable mutations.
|
29161592 |
2017 |
|
Neoplasms
|
0.060 |
Biomarker
|
group |
BEFREE |
GDF11 exhibits tumor suppressive properties in hepatocellular carcinoma cells by restricting clonal expansion and invasion.
|
30890427 |
2019 |
|
Neoplasms
|
0.060 |
Biomarker
|
group |
BEFREE |
These findings suggested that GDF11 acted as a tumor suppressor gene for pancreatic cancer.
|
30568460 |
2018 |
|
Neoplasms
|
0.060 |
Biomarker
|
group |
BEFREE |
We also demonstrate that CRC-associated human intestinal lymphatic endothelial cells regulate tumor cell growth via growth differentiation factor 11, a soluble matrisome component which in CRC patients was found to be associated with tumor progression.
|
30889293 |
2019 |
|
Cachexia
|
0.040 |
Biomarker
|
phenotype |
BEFREE |
Given this apparent contradiction in functionality, multiple independent labs sought to discern differences between the two factors and better elucidate age-related changes in circulating GDF11, with most failing to reproduce the initial finding of declining GDF11 levels, and, importantly, all subsequent studies examining the effects of GDF11 on skeletal muscle described an inhibitory effect on regeneration - and that higher doses induce skeletal muscle atrophy and cachexia.
|
31144559 |
2019 |
|
Cachexia
|
0.040 |
Biomarker
|
phenotype |
BEFREE |
Here, we find that elevated GDF11 causes signs of cachexia in mice: reduced food intake, body weight, and muscle mass.
|
29425507 |
2018 |
|
Cachexia
|
0.040 |
Biomarker
|
phenotype |
BEFREE |
The TGF-β family ligands myostatin, GDF11, and activins are negative regulators of skeletal muscle mass, which have been reported to primarily signal via the ActRIIB receptor on skeletal muscle and thereby induce muscle wasting described as cachexia.
|
29109273 |
2017 |
|
Alzheimer's Disease
|
0.030 |
Biomarker
|
disease |
BEFREE |
Growth differentiation factor 11 (GDF11) has an anti-inflammatory effect in the mouse model of atherosclerosis and Alzheimer's disease, but how GDF11 regulates intestinal inflammation during ulcerative colitis (UC) is poorly defined.
|
30188752 |
2018 |
|
Alzheimer's Disease
|
0.030 |
Biomarker
|
disease |
BEFREE |
Daily intravenous treatment with GDF11-injection can rejuvenate respects of cognition and cerebrovascular changes in AD mice.
|
29480172 |
2018 |
|
Alzheimer's Disease
|
0.030 |
Biomarker
|
disease |
BEFREE |
We suggest that alterations of GDF11 and Tregs are involved in AD progression and that rejuvenation of the immune system is a potential therapeutic strategy in AD.
|
26317549 |
2015 |
|
Malignant Neoplasms
|
0.030 |
Biomarker
|
group |
BEFREE |
Since its discovery in 1999, studies have shown the involvement of GDF11 in normal physiological processes, such as embryonic development and erythropoiesis, as well as in the pathophysiology of aging, cardiovascular disease, diabetes mellitus, and cancer.
|
29113418 |
2017 |
|
Malignant Neoplasms
|
0.030 |
Biomarker
|
group |
BEFREE |
This review is focused to present and analyze the recent findings in the emerging research field of GDF11 function in cancer and metabolism, and discusses the controversies surrounding the biology of this atypical growth factor.
|
31681577 |
2019 |
|
Cardiovascular Diseases
|
0.030 |
Biomarker
|
group |
BEFREE |
Since its discovery in 1999, studies have shown the involvement of GDF11 in normal physiological processes, such as embryonic development and erythropoiesis, as well as in the pathophysiology of aging, cardiovascular disease, diabetes mellitus, and cancer.
|
29113418 |
2017 |
|
Cardiovascular Diseases
|
0.030 |
Biomarker
|
group |
BEFREE |
Administration of GDF11 may be an efficacious therapy to protect against cardiovascular diseases in splenectomized patients.
|
27565745 |
2017 |
|
Colorectal Carcinoma
|
0.030 |
Biomarker
|
disease |
BEFREE |
We also demonstrate that CRC-associated human intestinal lymphatic endothelial cells regulate tumor cell growth via growth differentiation factor 11, a soluble matrisome component which in CRC patients was found to be associated with tumor progression.
|
30889293 |
2019 |