Level D· Scientific groundwork from lab and animal studiesNarrative ReviewEurope PMCOpen access

Interplay between PI3K/AKT pathway and heart disorders

Ghafouri-Fard S., Khanbabapour Sasi A., Hussen BM., Shoorei H., Siddiq A., Taheri M.

Narrative Review on Cardiovascular Disease, Chronic Inflammation, published in Mol Biol Rep (2022) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
Read the A–D evidence level guide

This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Narrative Review
Journal
Mol Biol Rep (2022)
Reported sample size
—
Source database
Europe PMC
PMID
35499687
PMCID
PMC9515023
DOI
10.1007/s11033-022-07468-0
Citations
137

Abstract (original English)

The PI3K/AKT signaling has crucial role in the regulation of numerous physiological functions through activation of downstream effectors and modulation of cell cycle transition, growth and proliferation. This pathway participates in the pathogenesis of several human disorders such as heart diseases through regulation of size and survival of cardiomyocytes, angiogenic processes as well as inflammatory responses. Moreover, PI3K/AKT pathway participates in the process of myocardial injury induced by a number of substances such as H 2 O 2 , Mercury, lipopolysaccharides, adriamycin, doxorubicin and epirubicin. In this review, we describe the contribution of this pathway in the pathoetiology of myocardial ischemia/reperfusion injury and myocardial infarction, heart failure, cardiac hypertrophy, cardiomyopathy and toxins-induced cardiac injury.

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is a narrative review: it collects no new patient data and does not systematically appraise evidence quality.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

How we grade evidence
Myocytes, CardiacHumansMyocardial Reperfusion InjuryHydrogen PeroxideMercuryDoxorubicinEpirubicinLipopolysaccharidesApoptosisProto-Oncogene Proteins c-akt

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