Evidence map›Paper›PMID 29355711›Full record

ReviewProgress in neurobiology

Implication of the Kallikrein-Kinin system in neurological disorders: Quest for potential biomarkers and mechanisms.

Amaly Nokkari, Hadi Abou-El-Hassan, Yehia Mechref, Stefania Mondello, Mark S Kindy, Ayad A Jaffa, Firas Kobeissy

Open access · greenAbstract readReview
In one paragraph

Review in Progress in neurobiology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
11.2field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

53 citing papers in PubMed, 1 synthesis or guideline pooled it, 126 citations in OpenAlex.

  1. Pooled it
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  4. Role of Kinin BCellular and molecular neurobiology · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 6 institutions in 3 countries.

Amaly NokkariDepartment of Biochemistry and Molecular Genetics, Faculty of Medicine, American University of Beirut, Lebanon.
Hadi Abou-El-HassanFaculty of Medicine, American University of Beirut Medical Center, Beirut, Lebanon.
Yehia MechrefDepartment of Chemistry and Biochemistry, Texas Tech University, Lubbock, TX, USA.
Stefania MondelloDepartment of Biomedical and Dental Sciences and Morphofunctional Imaging, University of Messina, Messina, Italy.
Mark S KindyDepartment of Pharmaceutical Science, College of Pharmacy, University of South Florida, Tampa, FL, USA; James A. Haley VA Medical Center, Tampa, FL, USA.
Ayad A JaffaDepartment of Biochemistry and Molecular Genetics, Faculty of Medicine, American University of Beirut, Lebanon; Department of Medicine, Medical University of South, Charleston, SC, USA. Electronic address: aj24@aub.edu.lb.
Firas KobeissyDepartment of Biochemistry and Molecular Genetics, Faculty of Medicine, American University of Beirut, Lebanon; Center for Neuroproteomics & Biomarkers Research, Department of Psychiatry, McKnight Brain Institute, University of Florida, Gainesville, FL, USA. Electronic address: firasko@ufl.edu.
American University of Beirut · LBAmerican University of Beirut Medical Center · LBJames A. Haley Veterans' Hospital · USTexas Tech University · USUniversity of Florida · USUniversity of Messina · IT

Funding

MECHANISMS OF VASCULAR DISEASE IN DIABETESR01HL077192 · NHLBI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI JAFFA, AYAD A · 2006 to 2017
$3.4M
Sensitive and Quantitative MS-bases Glycomic Mapping PlatformR01GM112490 · NIGMS · TEXAS TECH UNIVERSITY · PI MECHREF, YEHIA · 2014 to 2024
$3.2M
NHLBI NIH HHS R01 HL077192NIGMS NIH HHS R01 GM112490
6 · The paper itself

Abstract

Neurological disorders represent major health concerns in terms of comorbidity and mortality worldwide. Despite a tremendous increase in our understanding of the pathophysiological processes involved in disease progression and prevention, the accumulated knowledge so far resulted in relatively moderate translational benefits in terms of therapeutic interventions and enhanced clinical outcomes. Aiming at specific neural molecular pathways, different strategies have been geared to target the development and progression of such disorders. The kallikrein-kinin system (KKS) is among the most delineated candidate systems due to its ubiquitous roles mediating several of the pathophysiological features of these neurological disorders as well as being implicated in regulating various brain functions. Several experimental KKS models revealed that the inhibition or stimulation of the two receptors of the KKS system (B1R and B2R) can exhibit neuroprotective and/or adverse pathological outcomes. This updated review provides background details of the KKS components and their functions in different neurological disorders including temporal lobe epilepsy, traumatic brain injury, stroke, spinal cord injury, Alzheimer's disease, multiple sclerosis and glioma. Finally, this work will highlight the putative roles of the KKS components as potential neurotherapeutic targets and provide future perspectives on the possibility of translating these findings into potential clinical biomarkers in neurological disease.

Indexed as

AnimalsBiomarkersHumansKallikrein-Kinin SystemKininsNervous System DiseasesReceptors, BradykininSignal TransductionBiomarkersKininsReceptors, BradykininBiomarkersBradykininBrain injuryKallikrein-Kinin systemKininNeurological disorders

Identifiers

PMID29355711
PMCPMC6026079
OpenAlexW2788259524

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.