Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Lipid-Lowering Drugs: Statins and Miscellaneous Agents01:20

Lipid-Lowering Drugs: Statins and Miscellaneous Agents

1.8K
Hyperlipidemia, a medical condition often referred to as high cholesterol, is characterized by abnormally elevated levels of lipids in the bloodstream. When present in excess, these lipids, specifically cholesterol and triglycerides, can lead to serious health complications, often involving cardiovascular diseases. Illnesses like atherosclerosis, heart attacks, and pancreatitis have all been linked to untreated hyperlipidemia. This means controlling and regulating cholesterol and triglyceride...
1.8K
Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors01:20

Antiplatelet Drugs: Prostaglandin Synthesis, P2Y12 and Glycoprotein IIb/IIIa Inhibitors

1.5K
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.
Prostaglandin synthesis inhibitors, exemplified by the widely known aspirin, wield their power by irreversibly acetylating...
1.5K
Apoptosis01:30

Apoptosis

16.8K
Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size...
16.8K
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

9.2K
Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
9.2K
Structure and Function of Platelets01:18

Structure and Function of Platelets

4.6K
The cell fragments known as platelets are disc-shaped, with an average diameter of about 3 μm and a thickness of roughly 1 μm. They play a crucial role in the body's vascular clotting system, which also involves plasma proteins, blood cells, and blood vessel tissues.
Platelets are continually replenished, circulating in the bloodstream for 9-12 days before being removed by phagocytes, primarily in the spleen. A microliter of circulating blood contains between 150,000 and 450,000...
4.6K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Platelet RIP2 Limits Dense Granule Release and Thrombosis via DOCK8-Cdc42.

Arteriosclerosis, thrombosis, and vascular biology·2026
Same author

High-concentration estradiol promotes platelet activation and thrombosis through Src-ADP axis.

Translational research : the journal of laboratory and clinical medicine·2026
Same author

Role of albumin in regulating platelet function.

Frontiers in pharmacology·2026
Same author

Glycoprotein Ibα-Dependent Platelet Activation is Essential for Tumor Cell-Platelet Interaction and Experimental Metastasis.

MedComm·2025
Same author

BAD-Glucokinase Axis Regulates Platelet Activation and Thrombosis.

Arteriosclerosis, thrombosis, and vascular biology·2025
Same author

Iloprost Concentration-Dependently Attenuates Platelet Function and Apoptosis by Elevating PKA Activity.

Journal of cellular and molecular medicine·2025

Related Experiment Video

Updated: Mar 27, 2026

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation
04:37

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation

Published on: May 23, 2025

1.3K

Lovastatin induces platelet apoptosis.

Qing Zhao1, Ming Li2, Mengxing Chen1

  • 1Jiangsu Institute of Hematology, The First Affiliated Hospital of Soochow University, Collaborative Innovation Center of Hematology, Key Laboratory of Thrombosis and Hemostasis, Ministry of Health, Suzhou, China.

Environmental Toxicology and Pharmacology
|January 17, 2016
PubMed
Summary

Lovastatin, a common statin, induces programmed cell death in platelets by disrupting mitochondrial function. This impairs platelet aggregation and reduces circulating platelet counts, potentially explaining statin-associated bleeding risks.

Keywords:
ApoptosisHemorrhageLovastatinPlateletsThrombocytopenia

More Related Videos

Procoagulant Platelet Characterization by Measuring Phosphatidylserine Exposure and Microvesicle Release from Human Purified Platelets
05:49

Procoagulant Platelet Characterization by Measuring Phosphatidylserine Exposure and Microvesicle Release from Human Purified Platelets

Published on: November 29, 2024

1.3K
LC-MS Analysis of Human Platelets as a Platform for Studying Mitochondrial Metabolism
06:04

LC-MS Analysis of Human Platelets as a Platform for Studying Mitochondrial Metabolism

Published on: April 4, 2016

11.8K

Related Experiment Videos

Last Updated: Mar 27, 2026

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation
04:37

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation

Published on: May 23, 2025

1.3K
Procoagulant Platelet Characterization by Measuring Phosphatidylserine Exposure and Microvesicle Release from Human Purified Platelets
05:49

Procoagulant Platelet Characterization by Measuring Phosphatidylserine Exposure and Microvesicle Release from Human Purified Platelets

Published on: November 29, 2024

1.3K
LC-MS Analysis of Human Platelets as a Platform for Studying Mitochondrial Metabolism
06:04

LC-MS Analysis of Human Platelets as a Platform for Studying Mitochondrial Metabolism

Published on: April 4, 2016

11.8K

Area of Science:

  • Biochemistry
  • Pharmacology
  • Hematology

Background:

  • Statins are crucial for preventing atherosclerosis and treating coronary artery disease due to their effects on thrombosis.
  • The mechanisms behind statin-induced thrombocytopenia and hemorrhage remain unclear.
  • Platelet function and apoptosis are critical in thrombotic events.

Purpose of the Study:

  • To elucidate the mechanism by which lovastatin affects platelet function and survival.
  • To investigate the role of mitochondrial pathways and caspase activation in lovastatin-induced platelet apoptosis.
  • To determine if lovastatin impacts platelet activation or aggregation.

Main Methods:

  • Assessed mitochondrial inner transmembrane potential and caspase activation in lovastatin-treated platelets.
  • Measured P-selectin expression and PAC-1 binding to evaluate platelet activation.
  • Quantified collagen- and thrombin-induced platelet aggregation.
  • Utilized an integrin αIIbβ3 antagonist (RGDS) to study lovastatin's effects on apoptosis.
  • Administered lovastatin to mice to assess in vivo effects on circulating platelet counts.

Main Results:

  • Lovastatin dose-dependently induced mitochondrial depolarization, up-regulated Bak, down-regulated Bcl-XL, and activated caspases-3/8/9.
  • Lovastatin did not increase platelet surface P-selectin expression or PAC-1 binding.
  • Collagen- and thrombin-induced platelet aggregation were significantly reduced by lovastatin.
  • RGDS inhibited lovastatin-induced apoptosis in human platelets and integrin αIIbβ3-expressing CHO cells.
  • Lovastatin administration reduced circulating platelet counts in mice.

Conclusions:

  • Lovastatin induces caspase-dependent apoptosis in platelets via mitochondrial pathway disruption.
  • Lovastatin impairs platelet function and reduces circulating platelets in vivo without causing platelet activation.
  • These findings suggest a potential mechanism for statin-associated thrombocytopenia and hemorrhage.