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Please use this identifier to cite or link to this item: http://dspace.bits-pilani.ac.in:8080/jspui/handle/123456789/18541
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dc.contributor.authorMukherjee, Sudeshna-
dc.contributor.authorMajumder, Syamantak-
dc.contributor.authorChowdhury, Shibasish-
dc.contributor.authorChowdhury, Rajdeep-
dc.date.accessioned2025-04-03T10:36:10Z-
dc.date.available2025-04-03T10:36:10Z-
dc.date.issued2024-04-
dc.identifier.urihttps://www.biorxiv.org/content/10.1101/2024.04.23.590850v1.abstract-
dc.identifier.urihttp://dspace.bits-pilani.ac.in:8080/jspui/handle/123456789/18541-
dc.description.abstractHypoxia can trigger the activation of blood platelets, leading to thrombosis. If not addressed clinically, it can cause severe complications and fatal consequences as well. The current treatment regime for thrombosis is often palliative and includes long-term administration of anticoagulants, which has the risk of over-bleeding in injury and other secondary effects as well. This demands a deeper understanding of the process and exploration of an alternative therapeutic avenue. Interestingly, recent studies demonstrate that platelets though atypical and enucleated, possess components of autophagy machinery. This cellular homeostatic process though well-studied in non-platelet cells, is under-explored in platelets.en_US
dc.language.isoenen_US
dc.subjectBiologyen_US
dc.subjectAutophagyen_US
dc.subjectHypoxia imagingen_US
dc.subjectThrombosisen_US
dc.titleChloroquine attenuates hypoxia-mediated autophagy to curb thrombosis- an ex vivo and in vivo studyen_US
dc.typePreprinten_US
Appears in Collections:Department of Biological Sciences

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