metformin has been researched along with Progeria in 3 studies
Metformin: A biguanide hypoglycemic agent used in the treatment of non-insulin-dependent diabetes mellitus not responding to dietary modification. Metformin improves glycemic control by improving insulin sensitivity and decreasing intestinal absorption of glucose. (From Martindale, The Extra Pharmacopoeia, 30th ed, p289)
metformin : A member of the class of guanidines that is biguanide the carrying two methyl substituents at position 1.
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 |
|---|---|---|
| "Metformin has also recently been shown to beneficially alter gene splicing in normal humans." | 5.48 | Cellular stress and AMPK activation as a common mechanism of action linking the effects of metformin and diverse compounds that alleviate accelerated aging defects in Hutchinson-Gilford progeria syndrome. ( Finley, J, 2018) |
| "Metformin treatment partially restored normal nuclear phenotypes, delayed senescence, activated the phosphorylation of AMP-activated protein kinase and decreased reactive oxygen species formation in HGPS dermal fibroblasts." | 5.46 | Metformin alleviates ageing cellular phenotypes in Hutchinson-Gilford progeria syndrome dermal fibroblasts. ( Park, SK; Shin, OS, 2017) |
| "Metformin has also recently been shown to beneficially alter gene splicing in normal humans." | 1.48 | Cellular stress and AMPK activation as a common mechanism of action linking the effects of metformin and diverse compounds that alleviate accelerated aging defects in Hutchinson-Gilford progeria syndrome. ( Finley, J, 2018) |
| "Metformin treatment partially restored normal nuclear phenotypes, delayed senescence, activated the phosphorylation of AMP-activated protein kinase and decreased reactive oxygen species formation in HGPS dermal fibroblasts." | 1.46 | Metformin alleviates ageing cellular phenotypes in Hutchinson-Gilford progeria syndrome dermal fibroblasts. ( Park, SK; Shin, OS, 2017) |
| 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 |
|---|---|
| Finley, J | 2 |
| Park, SK | 1 |
| Shin, OS | 1 |
3 other studies available for metformin and Progeria
| Article | Year |
|---|---|
Cellular stress and AMPK activation as a common mechanism of action linking the effects of metformin and diverse compounds that alleviate accelerated aging defects in Hutchinson-Gilford progeria syndrome.
Topics: Aging; Alternative Splicing; AMP-Activated Protein Kinases; Animals; Cell Nucleus; Cellular Senescen | 2018 |
Alteration of splice site selection in the LMNA gene and inhibition of progerin production via AMPK activation.
Topics: Alternative Splicing; AMP-Activated Protein Kinases; Animals; Berberine; DNA, Mitochondrial; Enzyme | 2014 |
Metformin alleviates ageing cellular phenotypes in Hutchinson-Gilford progeria syndrome dermal fibroblasts.
Topics: AMP-Activated Protein Kinases; Animals; Cell Line; Cell Nucleus; Cell Proliferation; Cellular Senesc | 2017 |