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Mendeley readers
Attention Score in Context
| Title |
Oxidative stress-induced alterations in PPAR-γ and associated mitochondrial destabilization contribute to kidney cell apoptosis
|
|---|---|
| Published in |
American Journal of Physiology: Renal, Fluid & Electrolyte Physiology, August 2014
|
| DOI | 10.1152/ajprenal.00205.2014 |
| Pubmed ID | |
| Authors |
David M Small, Christudas Morais, Jeff S Coombes, Nigel C Bennett, David W Johnson, Glenda C Gobe |
| Abstract |
Mechanism(s) underlying renoprotection by peroxisome proliferator-activated receptor-gamma (PPARγ) agonists in diabetic and non-diabetic kidney disease are not well-understood. Mitochondrial dysfunction and oxidative stress contribute to kidney disease. PPARγ upregulates proteins required for mitochondrial biogenesis. Our aim was to determine whether PPARγ has a role in protecting kidney proximal tubular epithelium (PTE) against mitochondrial destabilisation and oxidative stress. HK-2 PTE cells were subjected to oxidative stress (0.2-1.0mM hydrogen peroxide/H2O2) for 2h and 18h and compared with untreated cells for: apoptosis, mitosis (morphology/biomarkers); cell viability (MTT); superoxide (dihydroethidium/DHE); mitochondrial function (MitoTracker Red; JC-1); ATP (luminescence); and mitochondrial ultrastructure. PPARγ, phospho-PPARγ, PPARγ-coactivator-1α (PGC-1α), Parkin (Park2), p62 and light chain3-beta (LC3β) were investigated using Western blots. PPARγ was modulated using the agonists rosiglitazone, pioglitazone and troglitazone. Mitochondrial destabilisation increased with H2O2 concentration: ATP decreased (2h, 18h; p<0.05); Mitotracker Red and JC-1 fluorescence indicated loss of mitochondrial membrane potential; and superoxide increased (18h; p<0.05). Electron microscopy indicated sparse mitochondria, with disrupted cristae. Mitophagy was evident at 2h (Park2, LC3β increased; p62 decreased). Impaired mitophagy was indicated by p62 accumulation at 18h (p<0.05). PPARγ expression decreased, phospho-PPARγ increased and PGC-1α decreased (2h), indicating aberrant PPARγ activation and reduced mitochondrial biogenesis. Cell viability decreased (2h & 18h; p<0.05). PPARγ agonists promoted further apoptosis. In summary, oxidative stress promoted mitochondrial destabilisation in kidney PTE, in association with increased PPARγ phosphorylation. PPARγ agonists failed to protect PTE. Despite positive effects in other tissues, PPARγ activation appears to be detrimental to kidney PTE health when oxidative stress induces damage. |
X Demographics
The data shown below were collected from the profiles of 3 X users who shared this research output. Click here to find out more about how the information was compiled.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| United States | 2 | 67% |
| Unknown | 1 | 33% |
Demographic breakdown
| Type | Count | As % |
|---|---|---|
| Members of the public | 2 | 67% |
| Scientists | 1 | 33% |
Mendeley readers
The data shown below were compiled from readership statistics for 42 Mendeley readers of this research output. Click here to see the associated Mendeley record.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 42 | 100% |
Demographic breakdown
| Readers by professional status | Count | As % |
|---|---|---|
| Student > Ph. D. Student | 8 | 19% |
| Researcher | 4 | 10% |
| Student > Bachelor | 4 | 10% |
| Student > Master | 4 | 10% |
| Lecturer | 3 | 7% |
| Other | 6 | 14% |
| Unknown | 13 | 31% |
| Readers by discipline | Count | As % |
|---|---|---|
| Agricultural and Biological Sciences | 7 | 17% |
| Medicine and Dentistry | 6 | 14% |
| Biochemistry, Genetics and Molecular Biology | 5 | 12% |
| Pharmacology, Toxicology and Pharmaceutical Science | 4 | 10% |
| Immunology and Microbiology | 2 | 5% |
| Other | 3 | 7% |
| Unknown | 15 | 36% |
Attention Score in Context
This research output has an Altmetric Attention Score of 2. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 18 July 2019.
All research outputs
#16,722,190
of 25,374,917 outputs
Outputs from American Journal of Physiology: Renal, Fluid & Electrolyte Physiology
#1,725
of 2,792 outputs
Outputs of similar age
#138,654
of 243,100 outputs
Outputs of similar age from American Journal of Physiology: Renal, Fluid & Electrolyte Physiology
#18
of 46 outputs
Altmetric has tracked 25,374,917 research outputs across all sources so far. This one is in the 32nd percentile – i.e., 32% of other outputs scored the same or lower than it.
So far Altmetric has tracked 2,792 research outputs from this source. They receive a mean Attention Score of 4.3. This one is in the 34th percentile – i.e., 34% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 243,100 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 40th percentile – i.e., 40% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 46 others from the same source and published within six weeks on either side of this one. This one has gotten more attention than average, scoring higher than 58% of its contemporaries.