ArticleThe American journal of pathology2004
Lack of the growth factor midkine enhances survival against cisplatin-induced renal damage.
Article in The American journal of pathology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 51 citations in OpenAlex.
- Midkine (MDK) in cancer and drug resistance: from inflammation to therapy.Discover oncology · 2025Review
- Midkine: A Cancer Biomarker Candidate and Innovative Therapeutic Approaches.European journal of breast health · 2024Article
- Elevated Midkine Serum Levels Are Associated with Long-Term Survival in Critically Ill Patients.International journal of molecular sciences · 2023Article
- Pro-Inflammatory Signalling PRRopels Cisplatin-Induced Toxicity.International journal of molecular sciences · 2022Review
- Development and validation of a PBRM1-associated immune prognostic model for clear cell renal cell carcinoma.Cancer medicine · 2021Article
- Midkine: Utility as a Predictor of Early Diabetic Nephropathy in Children with Type 1 Diabetes MellitusJournal of clinical research in pediatric endocrinology · 2021Article
- Midkine (MDK) growth factor: a key player in cancer progression and a promising therapeutic target.Oncogene · 2020Review
- Cisplatin-Induced Rodent Model of Kidney Injury: Characteristics and Challenges.BioMed research international · 2018Review
- From top to bottom: midkine and pleiotrophin as emerging players in immune regulation.Journal of leukocyte biology · 2017Review
- Efficacy of urinary midkine as a biomarker in patients with acute kidney injury.Clinical and experimental nephrology · 2017Observational
- (Mesenchymal) Stem Cell-Based Therapy in Cisplatin-Induced Acute Kidney Injury Animal Model: Risk of Immunogenicity and Tumorigenicity.Stem cells international · 2017Review
- Midkine as a potential diagnostic marker in epithelial ovarian cancer for cisplatin/paclitaxel combination clinical therapy.American journal of cancer research · 2015Article
- Measuring midkine: the utility of midkine as a biomarker in cancer and other diseases.British journal of pharmacology · 2014Review
- Midkine in nephrogenesis, hypertension and kidney diseases.British journal of pharmacology · 2014Review
- Restoring the renal microvasculature to treat chronic kidney disease.Nature reviews. Nephrology · 2012Review
- Growth factor Midkine is involved in the pathogenesis of renal injury induced by protein overload containing endotoxin.Clinical and experimental nephrology · 2011Article
- Midkine as a factor to counteract the deposition of amyloid β-peptide plaques: in vitro analysis and examination in knockout mice.International archives of medicine · 2011Article
- Midkine in inflammation.TheScientificWorldJournal · 2011Review
- Midkine: a promising molecule for drug development to treat diseases of the central nervous system.Current pharmaceutical design · 2011Review
- Midkine inhibitors: application of a simple assay procedure to screening of inhibitory compounds.International archives of medicine · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although cisplatin acts directly on proximal tubule epithelial cells and causes cell death, little is known regarding the biological significance of its secondary effects, such as inflammation. The growth factor midkine is highly expressed in the proximal tubule and exerts ambivalent activities as to cisplatin nephrotoxicity, ie, anti-apoptotic and chemotactic ones. Here we report that midkine-deficient mice show a significantly higher survival rate than wild-type mice. The levels of blood urea nitrogen and tubular degeneration and apoptosis were higher in wild-type mice despite the anti-apoptotic activity of midkine. We found that recruitment of neutrophils was more enhanced in wild-type mice, this being consistent with the chemotactic activity of midkine. Midkine expression in wild-type mice persisted for 24 hours, and then dramatically decreased. Preadministration of midkine anti-sense oligodeoxyribonucleotide to wild-type mice suppressed midkine expression, and consequently neutrophil infiltration. It is of note that neutrophil infiltration, apoptosis, and elevation of blood urea nitrogen became conspicuous sequentially, namely 1, 2, and 3 days after cisplatin administration, respectively. These findings suggest that early molecular events involving midkine induce inflammatory response and their circuits eventually enhance the death of the proximal tubule epithelial cells. The results indicate the crucial role of inflammation in cisplatin-induced renal damage, and provide a candidate molecular target for its prevention.
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.