Evidence map›Paper›PMID 24921004›Full record

ReviewWorld journal of biological chemistry2014

What have we learned about the kallikrein-kinin and renin-angiotensin systems in neurological disorders?

Maria da Graça Naffah-Mazzacoratti, Telma Luciana Furtado Gouveia, Priscila Santos Rodrigues Simões, Sandra Regina Perosa

Open access · diamondAbstract readReview
In one paragraph

Review in World journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

16 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
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  4. Review
  5. A modular map of Bradykinin-mediated inflammatory signaling network.Journal of cell communication and signaling · 2022
    Article
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  7. Article
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  11. Renin inhibitor aliskiren exerts beneficial effect on trabecular bone by regulating skeletal renin-angiotensin system and kallikrein-kinin system in ovariectomized mice.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2016
    Article
  12. Article
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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

4 authors at 1 institution in 1 country.

Maria da Graça Naffah-MazzacorattiMaria da Graça Naffah-Mazzacoratti, Telma Luciana Furtado Gouveia, Priscila Santos Rodrigues Simões, Sandra Regina Perosa, Department de Bioquímica and Departamento de Neurologia/Neurocirurgia, Universidade Federal de São Paulo (UNIFESP), São Paulo, SP 4039032, Brazil.
Telma Luciana Furtado GouveiaMaria da Graça Naffah-Mazzacoratti, Telma Luciana Furtado Gouveia, Priscila Santos Rodrigues Simões, Sandra Regina Perosa, Department de Bioquímica and Departamento de Neurologia/Neurocirurgia, Universidade Federal de São Paulo (UNIFESP), São Paulo, SP 4039032, Brazil.
Priscila Santos Rodrigues SimõesMaria da Graça Naffah-Mazzacoratti, Telma Luciana Furtado Gouveia, Priscila Santos Rodrigues Simões, Sandra Regina Perosa, Department de Bioquímica and Departamento de Neurologia/Neurocirurgia, Universidade Federal de São Paulo (UNIFESP), São Paulo, SP 4039032, Brazil.
Sandra Regina PerosaMaria da Graça Naffah-Mazzacoratti, Telma Luciana Furtado Gouveia, Priscila Santos Rodrigues Simões, Sandra Regina Perosa, Department de Bioquímica and Departamento de Neurologia/Neurocirurgia, Universidade Federal de São Paulo (UNIFESP), São Paulo, SP 4039032, Brazil.
Universidade Federal de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The kallikrein-kinin system (KKS) is an intricate endogenous pathway involved in several physiological and pathological cascades in the brain. Due to the pathological effects of kinins in blood vessels and tissues, their formation and degradation are tightly controlled. Their components have been related to several central nervous system diseases such as stroke, Alzheimer's disease, Parkinson's disease, multiple sclerosis, epilepsy and others. Bradykinin and its receptors (B1R and B2R) may have a role in the pathophysiology of certain central nervous system diseases. It has been suggested that kinin B1R is up-regulated in pathological conditions and has a neurodegenerative pattern, while kinin B2R is constitutive and can act as a neuroprotective factor in many neurological conditions. The renin angiotensin system (RAS) is an important blood pressure regulator and controls both sodium and water intake. AngII is a potent vasoconstrictor molecule and angiotensin converting enzyme is the major enzyme responsible for its release. AngII acts mainly on the AT1 receptor, with involvement in several systemic and neurological disorders. Brain RAS has been associated with physiological pathways, but is also associated with brain disorders. This review describes topics relating to the involvement of both systems in several forms of brain dysfunction and indicates components of the KKS and RAS that have been used as targets in several pharmacological approaches.

Indexed as

Alzheimer’s diseaseEpilepsyKallikrein-kinin systemNeurological disordersParkinson’s diseaseRenin-angiotensin system

Identifiers

PMID24921004
PMCPMC4050108
OpenAlexW7123135

What OpenQuestion holds

Textmetadata
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.