Inadequate blood supply persists in keloids

Koichi Ueda1, Yoshiko Yasuda, Eisuke Furuya

  • 1Department of Plastic and Reconstructive Surgery, Osaka Medical College, Osaka 569-8686, Japan. pla007@poh.osaka-med.ac.jp

Insights

Keloid tissue has high adenosine triphosphate (ATP) levels, likely from anaerobic glycolysis due to poor blood supply. Reduced vessel size and number in keloids may limit oxygen perfusion, persisting over time.

Area of Science:

  • Wound healing research
  • Dermatology
  • Biochemistry

Background:

  • Keloids exhibit persistently high adenosine triphosphate (ATP) levels.
  • Anaerobic glycolysis is a potential source of ATP in keloid tissue.

Purpose of the Study:

  • To investigate vascular characteristics and lactate concentrations in keloids compared to other scar types.
  • To elucidate the relationship between vascularity, lactate, and ATP production in keloids.

Main Methods:

  • Vessel counting in a defined area for keloids, hypertrophic scars, and atrophic scars.
  • Immunohistopathological measurement of internal vessel lumen cross-sectional areas.
  • Quantification of lactate concentrations in different scar types.

Main Results:

  • Keloids showed the lowest mean vessel count and mean internal vessel area.
  • Lactate concentration was highest in keloids (39.4 mmol/g protein) compared to red (23.8), pink (23.8), and white scars (13.3).
  • These findings suggest impaired oxygen perfusion in keloids.

Conclusions:

  • ATP in keloids is likely produced via anaerobic glycolysis.
  • Reduced and narrowed blood vessels contribute to inadequate and persistent blood supply in keloids.

Related Concept Videos

Regulation of Angiogenesis and Blood Supply01:24

Regulation of Angiogenesis and Blood Supply

Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits.  Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...
Phases of Wound Repair01:28

Phases of Wound Repair

Following injury, the integrity of the injured tissues must be reestablished. For example, in skin tissue, wound repair involves coordination among resident skin cells, blood mononuclear cells, extracellular matrix, growth factors, and cytokines to complete the healing cascade.
Formation of Blood Clot
In case of deep injuries, trauma to blood vessels results in blood loss. In the meantime, phospholipids released from the ruptured endothelial cellular membrane are converted into arachidonic...
Extrinsic and Intrinsic Pathways of Hemostasis01:20

Extrinsic and Intrinsic Pathways of Hemostasis

Blood clotting or coagulation involves extrinsic and intrinsic pathways, which ultimately merge into the common pathway, forming a fibrin clot.
The Extrinsic Pathway
The extrinsic pathway of coagulation is typically initiated by tissue damage that exposes blood to tissue factor (TF), a protein released by the damaged tissue cells outside the blood vessels—this interaction with TF triggers biochemical reactions involving specific clotting factors. The key player here is Factor VII, which forms a...
Disorders of Hemostasis01:24

Disorders of Hemostasis

Hemostasis, the process that stops bleeding after a blood vessel injury, is crucial for maintaining the integrity of the circulatory system. However, disorders of hemostasis can disrupt this delicate balance, leading to either excessive clotting or bleeding. These disorders can be broadly classified into thromboembolic disorders and bleeding disorders.
Thromboembolic Disorders
Two factors primarily cause thromboembolic conditions.
Healing II: Complications01:24

Healing II: Complications

Complications during healing arise when tissue repair is altered by local or systemic factors. These changes involve abnormal collagen deposition, altered biomechanics, and reduced vascular supply, impairing restoration of normal structure and function.Loss of FunctionScar tissue differs significantly from the original tissue it replaces. In the skin, fibrosis lacks adnexal structures such as hair follicles, sebaceous glands, and sweat glands. Their absence reduces tactile sensitivity, impairs...
Cirrhosis II: Pathophysiology01:24

Cirrhosis II: Pathophysiology

Cirrhosis is a progressive chronic liver injury caused by prolonged inflammation, excessive fibrotic remodeling, and impaired regeneration. Over time, repeated hepatic insults disrupt the liver’s architecture and function, leading to reduced blood flow, impaired bile drainage, and diminished metabolic capacity.Pathophysiology of cirrhosisCirrhosis arises from three main responses to chronic liver damage: inflammation, immune activation, and hepatocyte death. These processes lead to structural...