Page last updated: 2024-10-24

positive regulation of vascular wound healing

Definition

Target type: biologicalprocess

Any process that increases the rate, frequency, or extent of blood vessel formation when new vessels emerge from the proliferation of pre-existing blood vessels and contribute to the series of events that restore integrity to damaged vasculature. [GOC:rph]

Positive regulation of vascular wound healing is a complex biological process that involves a coordinated interplay of various cell types, signaling pathways, and extracellular matrix components. It ensures the efficient repair of damaged blood vessels and the restoration of vascular function. This intricate process begins with the detection of vascular injury, triggering a cascade of events that culminate in the formation of a stable blood clot, the recruitment of inflammatory cells, the proliferation and migration of vascular cells, and the remodeling of the damaged vessel.

Here's a detailed breakdown of the key events involved in positive regulation of vascular wound healing:

1. **Hemostasis and Clot Formation:**
- Upon vascular injury, the exposed subendothelial matrix triggers platelet activation and aggregation.
- Platelets release vasoconstrictors like thromboxane A2, leading to vasoconstriction and reducing blood flow to the injured site.
- The activated platelets also release growth factors and cytokines, initiating the inflammatory response and recruiting other cell types.
- The coagulation cascade is activated, culminating in the formation of a fibrin clot, which serves as a provisional matrix for wound healing and a barrier to further bleeding.

2. **Inflammation and Cellular Recruitment:**
- The initial vasoconstriction is followed by vasodilation, mediated by inflammatory mediators released by platelets and endothelial cells.
- This vasodilation facilitates the influx of neutrophils, macrophages, and other inflammatory cells to the injured site.
- Neutrophils play a crucial role in removing debris and pathogens from the wound, while macrophages clear apoptotic cells and release factors that promote angiogenesis and tissue regeneration.

3. **Angiogenesis and Vascular Remodeling:**
- The growth factors and cytokines released by platelets, macrophages, and endothelial cells promote the formation of new blood vessels (angiogenesis).
- These factors stimulate the proliferation and migration of endothelial cells, leading to the formation of capillary sprouts.
- The new blood vessels provide oxygen and nutrients to the healing tissue and remove metabolic waste.

4. **Extracellular Matrix Deposition and Remodeling:**
- As the wound heals, the provisional fibrin clot is gradually replaced by a more stable extracellular matrix (ECM) composed of collagen, elastin, and other proteins.
- Fibroblasts are recruited to the wound site and produce collagen and other ECM components, contributing to the strength and integrity of the repaired vessel.
- The ECM also provides structural support for the newly formed blood vessels and guides the orientation of vascular smooth muscle cells.

5. **Tissue Regeneration and Vessel Maturation:**
- As the wound heals, the inflammatory response subsides, and the newly formed blood vessels mature.
- The newly formed ECM undergoes remodeling, and the regenerated vessel acquires its normal structure and function.

6. **Key Signaling Pathways:**
- **VEGF Signaling:** Vascular endothelial growth factor (VEGF) plays a central role in angiogenesis. It stimulates the proliferation and migration of endothelial cells and the formation of new blood vessels.
- **PDGF Signaling:** Platelet-derived growth factor (PDGF) promotes the proliferation and migration of fibroblasts and smooth muscle cells, contributing to ECM deposition and vessel wall formation.
- **TGF-β Signaling:** Transforming growth factor beta (TGF-β) regulates ECM production, cell proliferation, and tissue remodeling. It plays a role in both wound healing and fibrosis.

7. **Regulation and Factors Influencing Wound Healing:**
- Wound healing is influenced by various factors, including age, nutritional status, smoking, diabetes, and the presence of infection.
- The body's ability to effectively regulate the complex processes involved in wound healing is essential for proper tissue repair and restoration of vascular function.

**Overall, positive regulation of vascular wound healing is a tightly orchestrated process that ensures the restoration of damaged blood vessels. This intricate process involves the coordinated actions of multiple cell types, signaling pathways, and ECM components, culminating in the formation of a stable and functional blood vessel.**'"

Proteins (1)

ProteinDefinitionTaxonomy
C-X-C chemokine receptor type 4A C-X-C chemokine receptor type 4 that is encoded in the genome of human. [PRO:WCB, UniProtKB:P61073]Homo sapiens (human)

Compounds (10)

CompoundDefinitionClassesRoles
zalcitabinezalcitabine : A pyrimidine 2',3'-dideoxyribonucleoside compound having cytosine as the nucleobase.

Zalcitabine: A dideoxynucleoside compound in which the 3'-hydroxy group on the sugar moiety has been replaced by a hydrogen. This modification prevents the formation of phosphodiester linkages which are needed for the completion of nucleic acid chains. The compound is a potent inhibitor of HIV replication at low concentrations, acting as a chain-terminator of viral DNA by binding to reverse transcriptase. Its principal toxic side effect is axonal degeneration resulting in peripheral neuropathy.
pyrimidine 2',3'-dideoxyribonucleosideantimetabolite;
antiviral drug;
HIV-1 reverse transcriptase inhibitor
plerixaforplerixafor : An azamacrocycle consisting of two cyclam rings connected by a 1,4-phenylenebis(methylene) linker. It is a CXCR4 chemokine receptor antagonist and a hematopoietic stem cell mobilizer. It is used in combination with grulocyte-colony stimulating factor (G-CSF) to mobilize hematopoietic stem cells to the perpheral blood for collection and subsequent autologous transplantation in patients with non-Hodgkin's lymphoma and multiple myeloma.

plerixafor: a bicyclam derivate, highly potent & selective inhibitor of HIV-1 & HIV-2
azacycloalkane;
azamacrocycle;
benzenes;
crown amine;
secondary amino compound;
tertiary amino compound
anti-HIV agent;
antineoplastic agent;
C-X-C chemokine receptor type 4 antagonist;
immunological adjuvant
benzylanilinebenzylaniline: major metabolite of antazoline; RN given refers to parent cpd
terephthalamidebenzenedicarboxamide
krh 1636KRH 1636: structure in first source
amd 8664
cyclo(d-tyrosyl-arginyl-arginyl-3-(2-naphthyl)alanyl-glycyl)oligopeptide
amd 070mavorixafor: a derivative of AMD3100; a CXCR4 blockeraminoquinoline
wz 811
tn14003TN14003: synthetic antagonist 14-mer peptide inhibiting metastasis in an animal model