Related Experiment Video

Updated: Mar 19, 2026

Enhancing the Engraftment of Human Induced Pluripotent Stem Cell-derived Cardiomyocytes via a Transient Inhibition of Rho Kinase Activity
08:00

Enhancing the Engraftment of Human Induced Pluripotent Stem Cell-derived Cardiomyocytes via a Transient Inhibition of Rho Kinase Activity

Published on: July 10, 2019

6.6K

MiR-28 inhibits cardiomyocyte survival through suppressing PDK1/Akt/mTOR signaling

Rui-Yao Zhu1, Di Zhang1, Han-Dong Zou1

  • 1Department of Critical Care Medicine, Renmin Hospital of Wuhan University, Wuhan, 430060, People's Republic of China.

In Vitro Cellular & Developmental Biology. Animal
|June 25, 2016
PubMed

Insights

MicroRNA-28 (miR-28) worsens heart cell death from oxidative stress by inhibiting the PDK1/Akt/mTOR pathway. Targeting miR-28 may protect hearts against ischemia-reperfusion injury.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Cell Biology

Background:

  • MicroRNAs regulate cell survival in heart disease.
  • Oxidative stress and apoptosis are key factors in heart ischemia-reperfusion injury.

Purpose of the Study:

  • To investigate the role of microRNA-28 (miR-28) in regulating cardiomyocyte survival under oxidative stress.
  • To elucidate the molecular mechanism by which miR-28 affects apoptosis in heart muscle cells.

Main Methods:

  • Upregulation of miR-28 in cardiomyocytes exposed to hydrogen peroxide (H2O2).
  • Assessing apoptosis levels with miR-28 gain and loss of function.
  • Analyzing the effect of miR-28 on the Akt/mammalian target of rapamycin (mTOR) signaling pathway.
  • Investigating the direct interaction between miR-28 and phosphoinositide-dependent kinase-1 (PDK1) using luciferase assays and Western blots.

Main Results:

  • miR-28 expression increased in cardiomyocytes treated with H2O2.
  • Increased miR-28 enhanced H2O2-induced apoptosis, while its inhibition partially rescued cells.
  • miR-28 significantly reduced the activity of the PDK1/Akt/mTOR signaling pathway.
  • PDK1 was identified as a direct and negative target of miR-28.

Conclusions:

  • miR-28 promotes oxidative stress-induced apoptosis in cardiomyocytes.
  • The mechanism involves the negative regulation of the PDK1/Akt/mTOR pathway by miR-28.
  • miR-28 represents a potential therapeutic target for reducing heart cell death in conditions like ischemia-reperfusion injury.
Keywords:
AktApoptosisHeartMicroRNAmTOR

More Related Videos

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes09:16

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes

Published on: June 3, 2018

7.8K
Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway07:15

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

1.0K

Related Concept Videos

PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
6.2K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
5.0K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

1.6K
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
6.1K
Inhibition of CDK Activity02:34

Inhibition of CDK Activity

5.6K
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
7.8K