ArticleCell cycle (Georgetown, Tex.)2018
Kidney atrophy vs hypertrophy in diabetes: which cells are involved?
Article in Cell cycle (Georgetown, Tex.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 2 citations in OpenAlex.
- Optimized renal protection with combined thymoquinone and glycine treatment: synergistic management of streptozotocin-induced nephropathy.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Article
- Exploring Therapeutic Potential ofCurrent topics in medicinal chemistry · 2026Article
- Short-Term Intake ofAntioxidants (Basel, Switzerland) · 2025Article
- Mapping the future: bibliometric insights into ferroptosis and diabetic nephropathy.Frontiers in physiology · 2025Review
- Hyperbaric oxygen therapy prevents epithelial atrophy in distal tubules and TGF-β1 overexpression in diabetic rat kidneys.Journal of molecular histology · 2024Article
- The value of tissue quantitative diffusion analysis of ultrasound elastography in the diagnosis of early-stage chronic kidney disease.BMC nephrology · 2024Article
- The transcriptome of early compensatory kidney growth reveals cell and time specific responses.iScience · 2024Article
- 24-h energy expenditure in people with type 1 diabetes: impact on equations for clinical estimation of energy expenditure.European journal of clinical nutrition · 2024Article
- Proximal tubule hypertrophy and hyperfunction: a novel pathophysiological feature in disease states.Clinical kidney journal · 2024Review
- Kidney shape statistical analysis: associations with disease and anthropometric factors.BMC nephrology · 2023Article
- Trunk muscle quality and quantity are associated with renal volume in nondiabetic people.Clinical kidney journal · 2023Article
- Super-Resolution Ultrasound Imaging of Renal Vascular Alterations in Zucker Diabetic Fatty Rats during the Development of Diabetic Kidney Disease.Diagnostics (Basel, Switzerland) · 2023Article
- Butyrate alleviates renal inflammation and fibrosis in a rat model of polycystic ovarian syndrome by suppression of SDF-1.BMC pharmacology & toxicology · 2023Article
- The UDPase ENTPD5 regulates ER stress-associated renal injury by mediating protein N-glycosylation.Cell death & disease · 2023Article
- PLVAP as an Early Marker of Glomerular Endothelial Damage in Mice with Diabetic Kidney Disease.International journal of molecular sciences · 2023Article
- The Molecular Mechanism of Renal Tubulointerstitial Inflammation Promoting Diabetic Nephropathy.International journal of nephrology and renovascular disease · 2023Review
- The Antihyperglycemic Effect of Crude Liang (Journal of nutrition and metabolism · 2023Article
- Use of haematological signatures in conjunction with conventional biomarkers to assess Reno-protective effects of Gedunin in diabetic nephropathy of Streptozotocin induced diabetic rats.Journal of diabetes and metabolic disorders · 2022Article
- Comparative Morphological, Metabolic and Transcriptome Analyses inFrontiers in cell and developmental biology · 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
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
One of the first structural changes in diabetic nephropathy (DN) is the renal enlargement. These changes resulted in renal hypertrophy in both glomerular and tubular cells. Shrink in the kidney size, which described as kidney atrophy resulted from the loss of nephrons or abnormal nephron function and lead to loss of the kidney function. On the other hand, increase in kidney size, which described as hypertrophy resulted from increase in proximal tubular epithelial and glomerular cells size. However overtime, tubular atrophy and tubulointerstitial fibrosis occurs as subsequent changes in tubular cell hypertrophy, which is associated with the infiltration of fibroblast cells into the tubulointerstitial space. The rate of deterioration of kidney function shows a strong correlation with the degree of tubulointerstitial fibrosis. A consequence of long-standing diabetes/hyperglycemia may lead to major changes in renal structure that occur but not specific only to nephropathy. Identifying type of cells that involves in renal atrophy and hypertrophy may help to find a therapeutic target to treat diabetic nephropathy. In summary, the early changes in diabetic kidney are mainly includes the increase in tubular basement membrane thickening which lead to renal hypertrophy. On the other hand, only renal tubule is subjected to apoptosis, which is one of the characteristic morphologic changes in diabetic kidney to form tubular atrophy at the late stage of diabetes.
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.