Updates in Kallikrein-Kinin System—KININ2022 Conference

Dear Colleagues,

Kinins are short-lived peptides that cause pain, arteriolar dilation, increased vascular permeability and contractions in smooth muscle. They are generated from kininogens through proteolysis by kallikreins. Together, these proteins and peptides, as well as their regulators, constitute the components of the kallikrein–kinin system (KKS).

Kinin production is dependent upon serine proteases, namely, plasma and tissue kallikreins. A prekallikrein is the precursor of plasma kallikrein that liberates bradykinin after it is activated by factor XIIa or enzymes. The activation and activity of both plasma kallikrein and factor XIIa are under the control of inhibitor C1, a serine protease inhibitor (serpin) protein. A deficiency of inhibitor C1 presents as a disorder of hereditary angioedema, a condition where there is less regulation of the production of vasoactive peptide bradykinin.

Kinins are inactivated by metallo-peptidases, such as: (i) carboxypeptidases, alias kininase I, that are present in two forms, circulating carboxypeptidase N and membrane-bound carboxypeptidase M, which remove C-terminal arginine residues of kinins; (ii) angiotensin-I-converting enzyme, alias kininase II, inactivating a number of peptide mediators, including bradykinin; (iii) aminopeptidase P that inactivates desArg⁹-kinins; (iv) neutral endopeptidase, which also deactivates kinins.

Kinin receptors B2 (constitutive) and B1 (inducible) are G-protein-coupled receptors that mediate activation signals through multiple tissues, including endothelial cells.

Kinins are directly, or indirectly, involved in many inflammatory diseases. If defects of the KKS in diseases are not generally recognized, the gain-of-function of one of the KKS component has been recognized to participate in hereditary angioedema. The KKS has been the subject of much research due to its relationship to inflammation and blood pressure systems. Kinins are generally considered to be inflammatory mediators, the accumulation of which causes the dilation of blood vessels, increased vascular permeability and pain, due to acting on phospholipase, with a subsequent release of arachidonic acid and prostaglandin production.

Similar to the KININ2022 conference, this research topic aims to expand on current knowledge data, recent progress and future plans in the field of kinins and the KKS, along with their relationships to diseases.

Within this Special Issue, we hope to publish original research articles, reviews, systematic reviews, mini reviews, methods, policy and practice reviews, hypotheses and theories, perspectives, clinical trials, case reports and community case studies, classifications, data reports, policy briefs, brief research reports, study protocols and Opinion articles, all of which would cover:

• Kallikrein–kinin system in biology;
• Kinin receptors: pharmacology, signalling and regulation;
• Animal models;
• Kallikrein–kinin system in diseases;
• Kallikrein–kinin system: drugs, inhibitors and antagonists.

We look forward to your participation. Thank you for your consideration.

Prof. Dr. Christian Drouet
Prof. Dr. Alvin Schmaier
Dr. Arije Ghannam
Guest Editors

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• kallikrein-kinin system
• kinin receptors
• kinin catabolism
• ACE inhibitors
• Kinin biomarkers
• kinin analysis
• hereditary angioedema
• C1 inhibitor and SERPING1 gene
• bladder detrusor muscle
• diabetic macular edema
• retinal pathologies
• host/parasite relationship