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Related Concept Videos

The JAK-STAT Signaling Pathway01:20

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Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
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Atherosclerosis I: Introduction01:30

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Atherosclerosis is a progressive disorder characterized by the buildup of plaques on the arterial inner wall, causing them to narrow and harden over time. These plaques comprise lipids, calcium, blood components, carbohydrates, and fibrous tissue. The process primarily affects the intima of large and medium-sized arteries, reducing blood flow in any artery.Etiology and risk factorsThe cause of atherosclerosis is multifactorial, involving a complex interplay among endothelial injury, lipid...
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Peripheral Artery Disease I: Introduction01:30

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Peripheral artery disease (PAD) predominantly results from atherosclerosis, which involves the accumulation of fatty deposits, or plaques, within the walls of arteries. This causes them to narrow and harden, significantly reducing blood flow. PAD predominantly affects the legs, particularly the arteries supplying the thighs and calves. In rare cases, it may involve other arteries, including those in the arms.Etiology of PAD:The principal cause of PAD is atherosclerosis, which results from fatty...
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Atherosclerosis II: Clinical Manifestations and Diagnostic Tests01:27

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Atherosclerosis is a progressive disorder that leads to the thickening and narrowing of arterial walls due to plaque buildup. This condition can cause various symptoms depending on the arteries affected:Coronary Artery Disease (CAD): This condition affects the coronary arteries and may lead to chest pain (angina), shortness of breath (dyspnea), heart attacks, and other heart disease symptoms.Cerebrovascular Disease: This affects blood flow to the brain, causing transient ischemic attacks (TIAs)...
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Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

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Antiplatelet drugs emerge as frontline defenders against the insidious threat of thromboembolic diseases, where abnormal clots obstruct vital blood vessels. These drugs stand as bulwarks, inhibiting platelet aggregation and clot formation, thereby mitigating the risk of life-threatening conditions like myocardial infarction, coronary artery disease, and thrombotic strokes.
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Related Experiment Video

Updated: Sep 11, 2025

A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
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Platelet Jak2 deficiency accelerates atherosclerosis with increased inflammatory response.

Daeun Kim1, Yu Zhe Li2, Jiaqi Yang1

  • 1Toronto General Hospital Research Institute, University Health Network, Toronto, Ontario, Canada.

The Journal of Biological Chemistry
|August 18, 2025
PubMed
Summary

Platelet Janus kinase 2 (Jak2) deficiency accelerates atherosclerosis by increasing inflammation and myeloid cell expansion. This suggests platelet Jak2 plays a protective role in cardiovascular disease progression.

Keywords:
Janus kinase (JAK)atherosclerosisbone marrowinflammationplatelet

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Area of Science:

  • Cardiovascular Biology
  • Immunology
  • Hematology

Background:

  • Cardiovascular disease (CVD) is a leading global cause of death, with atherosclerosis as its primary pathology.
  • Chronic inflammation is a key driver of atherosclerosis, involving signaling pathways like Janus kinase 2 (Jak2).
  • The Jak2V617F mutation is linked to clonal hematopoiesis and CVD risk, but platelet Jak2's role in atherosclerosis inflammation is unclear.

Purpose of the Study:

  • To investigate the in vivo role of platelet Janus kinase 2 (Jak2) in the development of atherosclerosis.
  • To determine if platelet Jak2 influences inflammatory cell recruitment and function during atherogenesis.

Main Methods:

  • Utilized ApoE-/- mice with platelet-specific Jak2 deficiency to model atherosclerosis.
  • Analyzed atherosclerotic lesion development in aortic roots and arches.
  • Assessed systemic inflammatory cell populations, bone marrow (BM)-derived macrophage inflammatory gene expression, and hematopoietic stem and progenitor cell (HSPC) expansion via flow cytometry.

Main Results:

  • Platelet Jak2-deficient mice exhibited accelerated atherosclerosis without metabolic changes.
  • Increased numbers of inflammatory leukocytes and platelets were observed systemically.
  • Bone marrow-derived macrophages showed heightened pro-inflammatory gene expression upon LPS stimulation.
  • Significant expansion of hematopoietic stem and progenitor cells was detected in the bone marrow.

Conclusions:

  • Platelet Janus kinase 2 (Jak2) plays a crucial role in attenuating atherosclerosis.
  • Platelet Jak2 likely exerts pleiotropic effects, including regulating inflammation in myeloid cells and influencing hematopoietic stem and progenitor cell populations.
  • Targeting platelet Jak2 may offer a novel therapeutic strategy for cardiovascular disease.