diphosphoric acid has been researched along with Progeria in 3 studies
diphosphoric acid : An acyclic phosphorus acid anhydride obtained by condensation of two molecules of phosphoric acid.
Progeria: An abnormal congenital condition, associated with defects in the LAMIN TYPE A gene, which is characterized by premature aging in children, where all the changes of cell senescence occur. It is manifested by premature graying; hair loss; hearing loss (DEAFNESS); cataracts (CATARACT); ARTHRITIS; OSTEOPOROSIS; DIABETES MELLITUS; atrophy of subcutaneous fat; skeletal hypoplasia; elevated urinary HYALURONIC ACID; and accelerated ATHEROSCLEROSIS. Many affected individuals develop malignant tumors, especially SARCOMA.
Excerpt | Relevance | Reference |
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"Excessive vascular calcification in Lmna(G609G) mice is caused by reduced extracellular accumulation of pyrophosphate that results from increased tissue-nonspecific alkaline phosphatase activity and diminished ATP availability caused by mitochondrial dysfunction in vascular smooth muscle cells." | 7.79 | Defective extracellular pyrophosphate metabolism promotes vascular calcification in a mouse model of Hutchinson-Gilford progeria syndrome that is ameliorated on pyrophosphate treatment. ( Acín-Pérez, R; Andrés, V; Enriquez, JA; López-Otín, C; Osorio, FG; Rivera-Torres, J; Villa-Bellosta, R, 2013) |
"Pyrophosphate deficiency may explain the excessive vascular calcification found in children with Hutchinson-Gilford progeria syndrome (HGPS) and in a mouse model of this disease." | 3.91 | ATP-based therapy prevents vascular calcification and extends longevity in a mouse model of Hutchinson-Gilford progeria syndrome. ( Villa-Bellosta, R, 2019) |
"Excessive vascular calcification in Lmna(G609G) mice is caused by reduced extracellular accumulation of pyrophosphate that results from increased tissue-nonspecific alkaline phosphatase activity and diminished ATP availability caused by mitochondrial dysfunction in vascular smooth muscle cells." | 3.79 | Defective extracellular pyrophosphate metabolism promotes vascular calcification in a mouse model of Hutchinson-Gilford progeria syndrome that is ameliorated on pyrophosphate treatment. ( Acín-Pérez, R; Andrés, V; Enriquez, JA; López-Otín, C; Osorio, FG; Rivera-Torres, J; Villa-Bellosta, R, 2013) |
Timeframe | Studies, this research(%) | All Research% |
---|---|---|
pre-1990 | 0 (0.00) | 18.7374 |
1990's | 0 (0.00) | 18.2507 |
2000's | 0 (0.00) | 29.6817 |
2010's | 3 (100.00) | 24.3611 |
2020's | 0 (0.00) | 2.80 |
Authors | Studies |
---|---|
Villa-Bellosta, R | 2 |
Rivera-Torres, J | 1 |
Osorio, FG | 1 |
Acín-Pérez, R | 1 |
Enriquez, JA | 1 |
López-Otín, C | 1 |
Andrés, V | 1 |
Leopold, JA | 1 |
3 other studies available for diphosphoric acid and Progeria
Article | Year |
---|---|
ATP-based therapy prevents vascular calcification and extends longevity in a mouse model of Hutchinson-Gilford progeria syndrome.
Topics: Adenosine Triphosphate; Alkaline Phosphatase; Animals; Antigens, CD; Aortic Diseases; Apyrase; Calci | 2019 |
Defective extracellular pyrophosphate metabolism promotes vascular calcification in a mouse model of Hutchinson-Gilford progeria syndrome that is ameliorated on pyrophosphate treatment.
Topics: Adenosine Triphosphate; Alkaline Phosphatase; Animals; Aorta; Cells, Cultured; Diphosphates; Disease | 2013 |
Vascular calcification: an age-old problem of old age.
Topics: Animals; Diphosphates; Male; Progeria; Vascular Calcification | 2013 |