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Controlling the receptor for advanced glycation end-products to conquer diabetic vascular complications.

Yamamoto Y, Yamamoto H - J Diabetes Investig (2012)

Bottom Line: Receptor-dependent mechanisms are involved in AGE-induced cellular dysfunction and tissue damage.The receptor for AGE (RAGE), originally an AGE-binding receptor, is now recognized as a member of pattern-recognition receptors and a pro-inflammatory molecular device that mediates danger signals to the body.Previous animal studies have shown RAGE dependent of diabetic vascular injuries.

View Article: PubMed Central - PubMed

Affiliation: Department of Biochemistry and Molecular Vascular Biology, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan.

ABSTRACT
Diabetic vascular complications, such as cardiovascular disease, stroke and microangiopathy, lead to high rates of morbidity and mortality in patients with long-term diabetes. Extensive intracellular and extracellular formation of advanced glycation end-products (AGE) is considered a causative factor in vascular injuries in diabetes. Receptor-dependent mechanisms are involved in AGE-induced cellular dysfunction and tissue damage. The receptor for AGE (RAGE), originally an AGE-binding receptor, is now recognized as a member of pattern-recognition receptors and a pro-inflammatory molecular device that mediates danger signals to the body. Previous animal studies have shown RAGE dependent of diabetic vascular injuries. Prophylactic and therapeutic strategies focusing on RAGE and its ligand axis will be of great importance in conquering diabetic vascular complications. (J Diabetes Invest, doi: 10.1111/j.2040-1124.2011.00191.x, 2012).

No MeSH data available.


Related in: MedlinePlus

 Receptor for advanced glycation end‐products (RAGE) and its multiple ligands in the development of diabetic vascular complications. Soluble RAGE (sRAGE) and endogenous soluble RAGE (esRAGE) might work as decoy receptors against ligand‐receptor interactions. This is adapted from our review paper96. AGE, advanced glycation end‐products; AOPP, advanced oxidation protein products; HMGB1, high‐mobility group box protein 1; NF‐κB, nuclear factor‐κB; PRR, pattern‐recognition receptors; TLR, toll‐like receptors.
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f2:  Receptor for advanced glycation end‐products (RAGE) and its multiple ligands in the development of diabetic vascular complications. Soluble RAGE (sRAGE) and endogenous soluble RAGE (esRAGE) might work as decoy receptors against ligand‐receptor interactions. This is adapted from our review paper96. AGE, advanced glycation end‐products; AOPP, advanced oxidation protein products; HMGB1, high‐mobility group box protein 1; NF‐κB, nuclear factor‐κB; PRR, pattern‐recognition receptors; TLR, toll‐like receptors.

Mentions: Endogenous and exogenous RAGE ligands other than AGE have been identified, including high‐mobility group box protein 1 (HMGB1), calcium‐binding S100 protein group, β2‐integrin Mac/CD11b, amyloid β peptide, β‐sheet fibrils, advanced oxidation protein products, complement C3a, lipopolysaccharides (LPS) and phosphatidylserine on the surface of apoptotic cells (Figure 2)38–44. RAGE is now considered to be a member of PRR like TLR; it actively participates in the interface of innate and adaptive immunity, inflammation, diabetic vascular complications and atherosclerosis (Figure 2).


Controlling the receptor for advanced glycation end-products to conquer diabetic vascular complications.

Yamamoto Y, Yamamoto H - J Diabetes Investig (2012)

 Receptor for advanced glycation end‐products (RAGE) and its multiple ligands in the development of diabetic vascular complications. Soluble RAGE (sRAGE) and endogenous soluble RAGE (esRAGE) might work as decoy receptors against ligand‐receptor interactions. This is adapted from our review paper96. AGE, advanced glycation end‐products; AOPP, advanced oxidation protein products; HMGB1, high‐mobility group box protein 1; NF‐κB, nuclear factor‐κB; PRR, pattern‐recognition receptors; TLR, toll‐like receptors.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4020727&req=5

f2:  Receptor for advanced glycation end‐products (RAGE) and its multiple ligands in the development of diabetic vascular complications. Soluble RAGE (sRAGE) and endogenous soluble RAGE (esRAGE) might work as decoy receptors against ligand‐receptor interactions. This is adapted from our review paper96. AGE, advanced glycation end‐products; AOPP, advanced oxidation protein products; HMGB1, high‐mobility group box protein 1; NF‐κB, nuclear factor‐κB; PRR, pattern‐recognition receptors; TLR, toll‐like receptors.
Mentions: Endogenous and exogenous RAGE ligands other than AGE have been identified, including high‐mobility group box protein 1 (HMGB1), calcium‐binding S100 protein group, β2‐integrin Mac/CD11b, amyloid β peptide, β‐sheet fibrils, advanced oxidation protein products, complement C3a, lipopolysaccharides (LPS) and phosphatidylserine on the surface of apoptotic cells (Figure 2)38–44. RAGE is now considered to be a member of PRR like TLR; it actively participates in the interface of innate and adaptive immunity, inflammation, diabetic vascular complications and atherosclerosis (Figure 2).

Bottom Line: Receptor-dependent mechanisms are involved in AGE-induced cellular dysfunction and tissue damage.The receptor for AGE (RAGE), originally an AGE-binding receptor, is now recognized as a member of pattern-recognition receptors and a pro-inflammatory molecular device that mediates danger signals to the body.Previous animal studies have shown RAGE dependent of diabetic vascular injuries.

View Article: PubMed Central - PubMed

Affiliation: Department of Biochemistry and Molecular Vascular Biology, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan.

ABSTRACT
Diabetic vascular complications, such as cardiovascular disease, stroke and microangiopathy, lead to high rates of morbidity and mortality in patients with long-term diabetes. Extensive intracellular and extracellular formation of advanced glycation end-products (AGE) is considered a causative factor in vascular injuries in diabetes. Receptor-dependent mechanisms are involved in AGE-induced cellular dysfunction and tissue damage. The receptor for AGE (RAGE), originally an AGE-binding receptor, is now recognized as a member of pattern-recognition receptors and a pro-inflammatory molecular device that mediates danger signals to the body. Previous animal studies have shown RAGE dependent of diabetic vascular injuries. Prophylactic and therapeutic strategies focusing on RAGE and its ligand axis will be of great importance in conquering diabetic vascular complications. (J Diabetes Invest, doi: 10.1111/j.2040-1124.2011.00191.x, 2012).

No MeSH data available.


Related in: MedlinePlus