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Kallikrein(K1)-kinin-kininase (ACE) and end-organ damage in ischemia and diabetes: therapeutic implications.
Biol Chem. 2016 12 01; 397(12):1217-1222.BC

Abstract

Genetic and pharmacological studies, clinical and experimental, focused on kallikrein-K1, kinin receptors and ACE/kininase II suggest that kinin release in the settings of ischemia or diabetes reduces organ damage, especially in the heart and kidney. Kinin bioavailability may be a limiting factor for efficacy of current kinin-potentiating drugs, like ACE inhibitors. Primary activation of kinin receptors by prototypic pharmacological agonists, peptidase-resistant, selective B1 or B2, displays therapeutic efficacy in experimental cardiac and peripheral ischemic and diabetic diseases. B1R agonism was especially efficient in diabetic animals and had no unwanted effects. Clinical development of kinin receptor agonists may be warranted.

Authors

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Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

27622831

Citation

Desposito, Dorinne, et al. "Kallikrein(K1)-kinin-kininase (ACE) and End-organ Damage in Ischemia and Diabetes: Therapeutic Implications." Biological Chemistry, vol. 397, no. 12, 2016, pp. 1217-1222.
Desposito D, Waeckel L, Potier L, et al. Kallikrein(K1)-kinin-kininase (ACE) and end-organ damage in ischemia and diabetes: therapeutic implications. Biol Chem. 2016;397(12):1217-1222.
Desposito, D., Waeckel, L., Potier, L., Richer, C., Roussel, R., Bouby, N., & Alhenc-Gelas, F. (2016). Kallikrein(K1)-kinin-kininase (ACE) and end-organ damage in ischemia and diabetes: therapeutic implications. Biological Chemistry, 397(12), 1217-1222. https://doi.org/10.1515/hsz-2016-0228
Desposito D, et al. Kallikrein(K1)-kinin-kininase (ACE) and End-organ Damage in Ischemia and Diabetes: Therapeutic Implications. Biol Chem. 2016 12 1;397(12):1217-1222. PubMed PMID: 27622831.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Kallikrein(K1)-kinin-kininase (ACE) and end-organ damage in ischemia and diabetes: therapeutic implications. AU - Desposito,Dorinne, AU - Waeckel,Ludovic, AU - Potier,Louis, AU - Richer,Christine, AU - Roussel,Ronan, AU - Bouby,Nadine, AU - Alhenc-Gelas,Francois, PY - 2016/06/10/received PY - 2016/08/19/accepted PY - 2016/9/14/pubmed PY - 2017/7/6/medline PY - 2016/9/14/entrez SP - 1217 EP - 1222 JF - Biological chemistry JO - Biol. Chem. VL - 397 IS - 12 N2 - Genetic and pharmacological studies, clinical and experimental, focused on kallikrein-K1, kinin receptors and ACE/kininase II suggest that kinin release in the settings of ischemia or diabetes reduces organ damage, especially in the heart and kidney. Kinin bioavailability may be a limiting factor for efficacy of current kinin-potentiating drugs, like ACE inhibitors. Primary activation of kinin receptors by prototypic pharmacological agonists, peptidase-resistant, selective B1 or B2, displays therapeutic efficacy in experimental cardiac and peripheral ischemic and diabetic diseases. B1R agonism was especially efficient in diabetic animals and had no unwanted effects. Clinical development of kinin receptor agonists may be warranted. SN - 1437-4315 UR - https://www.unboundmedicine.com/medline/citation/27622831/Kallikrein_K1__kinin_kininase__ACE__and_end_organ_damage_in_ischemia_and_diabetes:_therapeutic_implications_ L2 - https://www.degruyter.com/doi/10.1515/hsz-2016-0228 DB - PRIME DP - Unbound Medicine ER -