ReviewInternational journal of physiology, pathophysiology and pharmacology2016
Role of autophagy in megakaryocyte differentiation and platelet formation.
Review in International journal of physiology, pathophysiology and pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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
7 citing papers in PubMed, 17 citations in OpenAlex.
- Interactions between Plasmodium falciparum-infected red blood cells and their extracellular vesicles with megakaryocytes: implications for platelet-like particle formation.Malaria journal · 2025Article
- Inhibition of autophagy in platelets as a therapeutic strategy preventing hypoxia induced thrombosis.Scientific reports · 2025Article
- [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- Review
- Lack of COL6/collagen VI causes megakaryocyte dysfunction by impairing autophagy and inducing apoptosis.Autophagy · 2023Article
- Human platelets display dysregulated sepsis-associated autophagy, induced by altered LC3 protein-protein interaction of the Vici-protein EPG5.Autophagy · 2022Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagy is a conserved biological process for digestion and recycling of cytoplasmic constituents in eukaryotic cells. Autophagy may trigger cell death or promote cell survival following various forms of stress. The emerging roles of autophagy in megakaryopoiesis, thrombopoiesis, and platelet function have been uncovered using not only in vitro and in vivo genetic models, but also in clinical observations of autophagic structure in patients with thrombocytopenic disorders. Inhibition of autophagy in early stage of megakaryocyte differentiation appears to impede megakaryocyte maturation, reduce platelet formation, and affect platelet function, whereas autophagic deficiency in mature megakaryocytes gives rise to abnormal platelet activation and function without changing platelet size and number. On the other hand, induction of autophagy by rapamycin in megakaryocytes exhibited substantial therapeutic benefits in patients with immune thrombocytopenic purpura (ITP). This mini-review is to highlight recent progresses in understanding the regulation of autophagy in megakaryopoiesis, thrombopoiesis and platelet function to bridge the gap between autophagy and megakaryocyte/platelet pathophysiology.
Indexed as
Identifiers
27186320PMC4859876W2414980564What 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.