Evidence map›Paper›PMID 36700976›Full record

ReviewMolecular genetics and genomics : MGG2023

Role of c-Src and reactive oxygen species in cardiovascular diseases.

Misbah Hussain, Wajiha Ikram, Usama Ikram

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular genetics and genomics : MGG, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

14 citing papers in PubMed, 23 citations in OpenAlex.

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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

3 authors at 3 institutions in 1 country.

Misbah HussainDepartment of Biotechnology, University of Sargodha, Sargodha, 40120, Pakistan. misbah.hussain@uos.edu.pk.ORCID http://orcid.org/0000-0001-8825-917X
Wajiha IkramDepartment of Medicine, King Edward Medical University, Lahore, Pakistan.
Usama IkramDepartment of Medicine, Sheikh Khalifa Bin Zayed Al Nahyan Medical College, Lahore, Pakistan.
King Edward Medical University · PKShaikh Zayed Postgraduate Medical Institute · PKUniversity of Sargodha · PK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative stress, caused by the over production of oxidants or inactivity of antioxidants, can modulate the redox state of several target proteins such as tyrosine kinases, mitogen-activated protein kinases and tyrosine phosphatases. c-Src is one such non-receptor tyrosine kinase which activates NADPH oxidases (Noxs) in response to various growth factors and shear stress. Interaction between c-Src and Noxs is influenced by cell type and primary messengers such as angiotensin II, which binds to G-protein coupled receptor and activates the intracellular signaling cascade. c-Src stimulated activation of Noxs results in elevated release of intracellular and extracellular reactive oxygen species (ROS). These ROS species disturb vascular homeostasis and cause cardiac hypertrophy, coronary artery disease, atherosclerosis and hypertension. Interaction between c-Src and ROS in the pathobiology of cardiac fibrosis is hypothesized to be influenced by cell type and stimuli. c-Src and ROS have a bidirectional relationship, thus increased ROS levels due to c-Src mediated activation of Noxs can further activate c-Src by promoting the oxidation and sulfenylation of critical cysteine residues. This review highlights the role of c-Src and ROS in mediating downstream signaling pathways underlying cardiovascular diseases. Furthermore, due to the central role of c-Src in activation of various signaling proteins involved in differentiation, migration, proliferation, and cytoskeletal reorganization of vascular cells, it is presented as therapeutic target for treating cardiovascular diseases except cardiac fibrosis.

Indexed as

Cardiovascular DiseasesFibrosisGenes, srcHumansNADPH OxidasesOxidation-ReductionReactive Oxygen SpeciesSignal TransductionTyrosineNADPH OxidasesReactive Oxygen SpeciesTyrosineCardiovascular diseasesc-SrcNADPH oxidaseReactive oxygen speciesVascular dysfunction

Identifiers

PMID36700976
OpenAlexW4318067239

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.