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The Kallikrein-Kinin System: Current and Future Pharmacological Targets
Open accessAbstract
The kallikrein-kinin system is an endogenous metabolic cascade, triggering of which results in the release of vasoactive kinins (bradykinin-related peptides). This complex system includes the precursors of kinins known as kininogens and mainly tissue and plasma kallikreins. The pharmacologically active kinins, which are often considered as either proinflammatory or cardioprotective, are implicated in many physiological and pathological processes. The interest of the various components of this multi-protein system is explained in part by the multiplicity of its pharmacological activities, mediated not only by kinins and their receptors, but also by their precursors and their activators and the metallopeptidases and the antiproteases that limit their activities. The regulation of this system by serpins and the wide distribution of the different constituents add to the complexity of this system, as well as its multiple relationships with other important metabolic pathways such as the renin-angiotensin, coagulation, or complement pathways. The purpose of this review is to summarize the main properties of this kallikrein-kinin system and to address the multiple pharmacological interventions that modulate the functions of this system, restraining its proinflammatory effects or potentiating its cardiovascular properties.
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“During ACE inhibition, bradykinin is primarily inactivated by aminopeptidase P (APP).”
From Sex-dependent and race-dependent association of XPNPEP2 C-2399A polymorphism with angiotensin-converting enzyme inhibitor-associated angioedema (2010) · cites this paper as [8]
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Metadata
- Authors
- Moreau, M. E., Garbacki, N., Molinaro, G., Brown, N. J., Marceau, F., & Adam, A.
- Affiliations
- Université de Montréal (CA)
- University of Liège (BE)
- Vanderbilt University (US)
- Centre hospitalier universitaire de Québec (CA)
- Venue
- Journal of Pharmacological Sciences
- Publisher
- Japanese Pharmacological Society
- Published
- 2005
- Volume
- 99
- Issue
- 1
- Pages
- 6-38
- ISSN
- 1347-8613 (ISSN-L)
- 1347-8648
- OpenAlex
- W1967632907
- Semantic Scholar
- 11ef9af17a7b09227baf4d743022d17406b6c59a
- Cited by
- 457
- References
- 324
- Citations by year
- 2026: 2 · 2025: 9 · 2024: 19 · 2023: 14 · 2022: 7 · 2021: 20 · 2020: 24 · 2019: 9 · 2018: 20 · 2017: 13 · 2016: 29 · 2015: 23 · 2014: 24 · 2013: 37 · 2012: 33
- FWCI
- 4.07
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Pharmacological Sciences (publishedVersion)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- ORBi (University of Liège) (submittedVersion, other-oa)
- Funders
- National Institutes of Health
- National Heart, Lung, and Blood Institute (R01HL079184)
- Topics
- Health Sciences › Medicine › Hematology › Coagulation, Bradykinin, Polyphosphates, and Angioedema
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Pineapple and bromelain studies
- Life Sciences › Immunology and Microbiology › Immunology › Complement system in diseases
- Keywords
- kallikrein-kinin system, bradykinin, kininogen, tissue kallikrein, plasma kallikrein, kinin receptors, metalloproteinases, antiproteases, serpins, pro-inflammatory effects, cardioprotection, renin-angiotensin system, coagulation, complement system, therapeutic target
- MeSH terms
- Angioedema, Angiotensin-Converting Enzyme Inhibitors, Animals, Bradykinin, Cardiovascular Diseases, Complement C1 Inactivator Proteins, Humans, Inflammation, Kallikreins, Aprotinin, Kidney Diseases, Peptidyl-Dipeptidase A, Kinins, Polymorphism, Genetic, Pyridines, Thiazepines, Neprilysin, Serpins, Randomized Controlled Trials as Topic, Kallikrein-Kinin System, Receptor, Bradykinin B2, Receptor, Bradykinin B1, Complement C1 Inhibitor Protein, Bradykinin B2 Receptor Antagonists
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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