ArticleMolecular medicine reports2018
PGC-1α ameliorates kidney fibrosis in mice with diabetic kidney disease through an antioxidative mechanism.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
40 citing papers in PubMed, 47 citations in OpenAlex.
- Exploring the renoprotective potential of Beta vulgaris in diabetic nephropathy: an integrated network pharmacology, molecular docking and dynamics simulation study.Molecular diversity · 2026Article
- Review
- Diabetic kidney disease: emerging mechanistic and nutritional perspectives from the Mediterranean diet-mitochondria axis. A narrative review.The journal of nutrition, health & aging · 2026Review
- Poria cocos Polysaccharides Protect Against Contrast-Induced Renal Injury Through Activating CaMKK2/AMPK/PGC-1α Signaling Pathway.Phytotherapy research : PTR · 2026Article
- Roles of the peroxisome proliferator-activated receptors (PPARs) in the pathogenesis of diabetic kidney disease (DKD).Cell death discovery · 2026Review
- Article
- Unraveling the role of mitochondrial dysfunction in diabetic kidney disease: insights and interventions.Frontiers in pharmacology · 2025Review
- Omega-3 Fatty Acids Modify Drp1 Expression and Activate the PINK1-Dependent Mitophagy Pathway in the Kidney and Heart of Adenine-Induced Uremic Rats.Biomedicines · 2024Article
- Oxidative Stress: A Culprit in the Progression of Diabetic Kidney Disease.Antioxidants (Basel, Switzerland) · 2024Review
- Peroxisome proliferator-activated receptor gamma coactivator-1 (PGC-1) family in physiological and pathophysiological process and diseases.Signal transduction and targeted therapy · 2024Review
- PGC1-α in diabetic kidney disease: unraveling renoprotection and molecular mechanisms.Molecular biology reports · 2024Review
- Effects of Exercise Training on Mitochondrial Fatty Acid β-Oxidation in the Kidneys of Dahl Salt-Sensitive Rats.International journal of molecular sciences · 2023Article
- From Physiology to Pathology: The Role of Mitochondria in Acute Kidney Injuries and Chronic Kidney Diseases.Kidney diseases (Basel, Switzerland) · 2023Review
- Mitochondrial quality control and its emerging role in the pathogenesis of diabetic kidney disease.Kidney research and clinical practice · 2023Article
- PGC-1α Is a Master Regulator of Mitochondrial Lifecycle and ROS Stress Response.Antioxidants (Basel, Switzerland) · 2023Review
- Population Dynamics, Plasma Cytokines and Platelet Centrifugation: Technical and Sociodemographic Aspects of 'Ovarian Rejuvenation'.Clinics and practice · 2023Article
- The Mitochondrion: A Promising Target for Kidney Disease.Pharmaceutics · 2023Review
- Mechanisms of mitochondrial respiratory adaptation.Nature reviews. Molecular cell biology · 2022Review
- Druggability of lipid metabolism modulation against renal fibrosis.Acta pharmacologica Sinica · 2022Review
- PGC-1α inhibits the NLRP3 inflammasome via preserving mitochondrial viability to protect kidney fibrosis.Cell death & disease · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The production of reactive oxygen species (ROS) is a common phenomenon in podocyte impairment, which leads to the irreversible progression of chronic kidney diseases, such as diabetic kidney disease (DKD). Previous research has indicated that peroxisome proliferator‑activated receptor γ (PPARγ) coactivator‑1α (PGC‑1α) participates in mitochondrial biogenesis and energy metabolism in certain mitochondria‑enriched cells, including myocardial and skeletal muscle cells. Therefore, we hypothesized that PGC‑1α may be a protective nuclear factor against energy and oxidative stress in DKD. To investigate this hypothesis, db/db diabetic mice were used to establish a DKD model and the PPARγ agonist rosiglitazone was employed to induce PGC‑1α expression in vivo. Additionally, immortalized mouse podocytes and SV40 MES 13 renal mesangial cells were utilized for in vitro experiments. The expression levels of PGC‑1α and genes associated with kidney and cell injury were determined by western blotting or reverse transcription-quantitative polymerase chain reaction and intracellular ROS levels were assessed by 2',7'-dichlorodihydrofluorescein diacetate. The results of the present study demonstrated that endogenous PGC‑1α expression exhibited protective effects against oxidative stress, glomerulosclerosis and tubulointerstitial fibrosis in experimental DKD. These results indicated a potential role of PGC‑1α in the amelioration of key pathophysiological features of DKD and provided evidence for PGC‑1α as a potential therapeutic target in DKD.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.