ArticleEMBO molecular medicine2016
Inducing mitophagy in diabetic platelets protects against severe oxidative stress.
Article in EMBO molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 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
76 citing papers in PubMed, 130 citations in OpenAlex.
- Trial
- Platelet Rubicon Bidirectional Regulation of GPVI and Integrin αIIbβ3 Signaling Mitigates Stroke Infarction Without Compromising Hemostasis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Platelet Autophagy as a Druggable Intracellular Pathway: Therapeutic Opportunities in Thromboinflammatory Diseases.Pharmaceutics · 2026Review
- Role of Rubicon in platelets: a promoter of thrombosis but not an autophagy repressor.Blood advances · 2026Article
- Platelet mitochondria dysfunction in diabetes mellitus: mechanisms and therapeutic implications.Frontiers in pharmacology · 2026Review
- Sir2 regulates selective autophagy in stationary-phase yeast cells.Microbial cell (Graz, Austria) · 2026Article
- Redox Control in Platelet Activity and Therapy.Antioxidants (Basel, Switzerland) · 2025Review
- TNF-α impairs platelet function by inhibiting autophagy and disrupting metabolism via syntaxin 17 downregulation.The Journal of clinical investigation · 2025Article
- Platelet Extracellular Vesicles as Natural Delivery Vehicles for Mitochondrial Dysfunction Therapy?ACS biomaterials science & engineering · 2025Review
- PAK4 promotes the cytoskeletal organization and meiotic maturation via phosphorylating DDX17 in oocyte.Cell communication and signaling : CCS · 2025Article
- Sulforaphane attenuates aldose reductase-mediated platelet dysfunction in high glucose-stimulated human platelets via downregulation of the Src/ROS/p53 signaling pathway.Frontiers in nutrition · 2025Article
- Demographic diversity in platelet function and response to antiplatelet therapy.Trends in pharmacological sciences · 2025Review
- Understanding the Role of Oxidative Stress in Platelet Alterations and Thrombosis Risk among Frail Older Adults.Biomedicines · 2024Review
- Platelets in Kawasaki disease: mediators of vascular inflammation.Nature reviews. Rheumatology · 2024Review
- Mitophagy-related regulated cell death: molecular mechanisms and disease implications.Cell death & disease · 2024Review
- Methionine sulfoxide reductase B2 protects against cardiac complications in diabetes mellitus.Diabetology & metabolic syndrome · 2024Article
- Sirt3 Protects Retinal Pigment Epithelial Cells From High Glucose-Induced Injury by Promoting Mitophagy Through the AMPK/mTOR/ULK1 Pathway.Translational vision science & technology · 2024Article
- Mitofusin-2 Regulates Platelet Mitochondria and Function.Circulation research · 2024Article
- Platelet Mitochondrial Fusion and Function in Vascular Integrity.Circulation research · 2024Article
- Structural analysis of platelet fragments and extracellular vesicles produced by apheresis platelets during storage.Blood advances · 2024Article
16 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 1 institution in 2 countries.
Funding
Abstract
Diabetes mellitus (DM) is a growing international concern. Considerable mortality and morbidity associated with diabetes mellitus arise predominantly from thrombotic cardiovascular events. Oxidative stress-mediated mitochondrial damage contributes significantly to enhanced thrombosis in DM A basal autophagy process has recently been described as playing an important role in normal platelet activation. We now report a substantial mitophagy induction (above basal autophagy levels) in diabetic platelets, suggesting alternative roles for autophagy in platelet pathology. Using a combination of molecular, biochemical, and imaging studies on human DM platelets, we report that platelet mitophagy induction serves as a platelet protective mechanism that responds to oxidative stress through JNK activation. By removing damaged mitochondria (mitophagy), phosphorylated p53 is reduced, preventing progression to apoptosis, and preserving platelet function. The absence of mitophagy in DM platelets results in failure to protect against oxidative stress, leading to increased thrombosis. Surprisingly, this removal of damaged mitochondria does not require contributions from transcription, as platelets lack a nucleus. The considerable energy and resources expended in "prepackaging" the complex mitophagy machinery in a short-lived normal platelet support a critical role, in anticipation of exposure to oxidative stress.
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.