Related Experiment Video
Updated: Apr 17, 2026

08:23
Characterization of Sickling During Controlled Automated Deoxygenation with Oxygen Gradient Ektacytometry
Published on: November 5, 2019
10.5K
Attenuating a sickle cell crisis with annexin V
1Manatee Memorial Hospital, Bradenton, FL, USA.
Medical Hypotheses
|February 11, 2015
Summary
Sickle cell crises are painful but usually resolve. Annexin V may help end crises faster by blocking phosphatidylserine on red blood cells, preventing clots.
Area of Science:
- Hematology
- Vascular Biology
- Biochemistry
Background:
- Sickle cell disease (SCD) involves painful crises that resolve spontaneously.
- An imbalance between steady state SCD and crisis state suggests potential therapeutic interventions.
- Prematurely senescent erythrocytes with exposed phosphatidylserine (PS) are implicated in SCD pathophysiology.
Purpose of the Study:
- To investigate the potential of Annexin V as a therapeutic agent to hasten the termination of sickle cell crises.
- To explore the role of phosphatidylserine (PS) exposure on erythrocytes in sickle cell crisis initiation and propagation.
Main Methods:
- The study focuses on the interaction of Annexin V with phosphatidylserine (PS) on senescent erythrocytes.
- Investigating how Annexin V binding to PS may inhibit erythrocyte adhesion and coagulation cascade initiation.
Main Results:
- In sickle cell disease (SCD), a high percentage of erythrocytes prematurely senesce and expose phosphatidylserine (PS).
- Exposed PS on circulating sickle erythrocytes promotes adhesion to the endothelium and initiates the coagulation cascade.
- Annexin V has a high affinity for PS, potentially shielding it and blocking these pathological processes.
Conclusions:
- Annexin V's ability to bind PS suggests it could act as a therapeutic shield.
- Targeting PS-exposing erythrocytes with Annexin V may offer a novel strategy to terminate sickle cell crises.
- This approach could help stabilize the physiologic balance disrupted during sickle cell crises.
More Related Videos
Related Concept Videos
Cytotoxic Edema: Pathophysiology
1
Cytotoxic edema is a form of cerebral edema characterized by intracellular swelling of neurons, astrocytes, and other glial cells. It develops when the mechanisms responsible for maintaining ionic gradients across the cell membrane become impaired. Under normal physiological conditions, the sodium–potassium ATPase actively transports sodium ions out of the cell and potassium ions into the cell, preserving osmotic balance and enabling electrical signaling. This pump requires a continuous...
1
Cellular Injury IlI: Cellular Death
2
Cell death is the irreversible loss of cellular structure and function, representing the final stage of severe injury. It plays a key role in both normal physiology and disease.Types of Cell DeathThe two main types are necrosis and apoptosis, though others like necroptosis and pyroptosis also exist.Necrosis:Necrosis is an unregulated form of cell death caused by severe injury such as trauma, toxins, or ischemia. It is characterized by cell swelling, membrane loss, rupture, and leakage of...
2
Cellular Injury V: Apoptosis and Autophagy
5
Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
5
The Extrinsic Apoptotic Pathway
9.4K
The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
9.4K
Cellular Injury IV: Necrosis
4
Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...
4
Acute Kidney Injury II: Pathophysiology
2.1K
Acute kidney injury (AKI) causes are categorized into three primary categories based on the location of the injury: prerenal, intrarenal (or intrinsic), and postrenal causes. This classification guides clinical management and illustrates how different pathways can impair kidney function.Etiology and Pathophysiology of Acute Kidney Injury1. Prerenal causesEtiology: Prerenal Acute Kidney Injury, the most common type, occurs when reduced blood flow to the kidneys decreases filtration capacity...
2.1K

