Related Experiment Video

Updated: Jun 30, 2025

Molecular Modulation by Lentivirus-Delivered Specific shRNAs in Endoplasmic Reticulum Stressed Neurons
10:50

Molecular Modulation by Lentivirus-Delivered Specific shRNAs in Endoplasmic Reticulum Stressed Neurons

Published on: April 24, 2021

1.0K

Omilancor mitigates the senescence of nucleus pulposus cells induced by DDP through targeting MAP2K6

Fang Yafeng1, Shi Xinpeng1, Wei Rong1

  • 1Luoyang Central Hospital Affiliated to Zhengzhou University, Luoyang, Henan, China.

Aging
|March 22, 2024
PubMed
Abstract

Insights

Omilancor shows promise for treating Intervertebral Disc Degeneration (IDD). By targeting MAP2K6, it effectively inhibits cellular senescence and alleviates disc degeneration in a rat model.

Area of Science:

  • Biomedical Research
  • Molecular Biology
  • Regenerative Medicine

Background:

  • Intervertebral Disc Degeneration (IDD) is a significant cause of back pain.
  • Cellular senescence is implicated in the progression of IDD.
  • MAP2K6 is identified as a key regulator in IDD pathogenesis.

Purpose of the Study:

  • To investigate Omilancor as a potential therapeutic agent for IDD.
  • To explore the role of MAP2K6 in IDD and its modulation by Omilancor.
  • To assess the efficacy of Omilancor in preclinical models of IDD.

Main Methods:

  • Analysis of mRNA microarray datasets to identify key regulators in IDD.
  • In vitro studies using cisplatin (DDP) to induce cellular senescence and upregulate MAP2K6.
  • Molecular docking to identify Omilancor's binding affinity to MAP2K6.
  • Evaluation of Omilancor's effect on IVD degeneration in a rat model.

Main Results:

  • MAP2K6 was identified as a critical factor in IDD progression.
  • Cisplatin treatment upregulated MAP2K6 and induced cellular senescence in vitro.
  • Omilancor demonstrated binding to MAP2K6, inhibiting DDP-induced senescence.
  • Omilancor administration significantly reduced IVD degeneration in a rat model.

Conclusions:

  • Omilancor effectively targets MAP2K6 to counteract cellular senescence.
  • Omilancor presents a promising therapeutic strategy for Intervertebral Disc Degeneration.
  • Targeting MAP2K6-mediated senescence offers a novel approach for IDD treatment.
Keywords:
MAP2K6Omilancorcellular senescenceintervertebral disc degeneration

More Related Videos

Modeling Age-Associated Neurodegenerative Diseases in Caenorhabditis elegans07:04

Modeling Age-Associated Neurodegenerative Diseases in Caenorhabditis elegans

Published on: August 15, 2020

5.4K
Cell Death Associated with Abnormal Mitosis Observed by Confocal Imaging in Live Cancer Cells15:53

Cell Death Associated with Abnormal Mitosis Observed by Confocal Imaging in Live Cancer Cells

Published on: August 21, 2013

15.0K

Related Concept Videos

Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
4.5K
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
5.5K
Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size...
11.4K
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
6.5K
Mitochondria01:37

Mitochondria

Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...
12.4K
Nonsense-mediated mRNA Decay02:27

Nonsense-mediated mRNA Decay

The Upf proteins that carry out nonsense-mediated decay (NMD) are found in all eukaryotic organisms, including humans. Each protein has an individual role, but they need to work in collaboration. Upf1 is an ATP-dependent RNA helicase that unwinds the RNA helix. Because Upf1 can unwind any RNA, Upf2 and Upf3 are required to help Upf1 discriminate between nonsense and normal mRNAs.
Usually, Upf3 binds to an Exon Junction Complex (EJC) at mRNA splice sites. If a ribosome fully translates the mRNA,...
10.6K