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Related Concept Videos

Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

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Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
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Once a ligand binds to a receptor, the signal is transmitted through the membrane and into the cytoplasm. The continuation of a signal in this manner is called signal transduction. Signal transduction only occurs with cell-surface receptors, which cannot interact with most components of the cell, such as DNA. Only internal receptors can interact directly with DNA in the nucleus to initiate protein synthesis. When a ligand binds to its receptor, conformational changes occur that affect the...
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The physiological function of a cell and cellular communication are outcomes of a range of extrinsic signals, intracellular signaling pathways, and cellular responses. No two cell types express the same repertoire of signaling components. Receptors are highly selective for their cognate ligands, but once activated, they can alter multiple cellular processes such as DNA transcription, protein synthesis, and metabolic activity. 
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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...
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A signaling cascade is a series of events that facilitates the transmission of information within or between cells, culminating in a targeted response in the recipient cell. As chemical messengers, hormones are pivotal in initiating and modulating these intricate signaling cascades based on their solubility.
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When a ligand binds to a cell-surface receptor, the receptor's intracellular domain changes shape, which may either activate its enzyme function or allow its binding to other molecules. The initial signal is amplified by most signal transduction pathways. This means that a single ligand molecule can activate multiple molecules of a downstream target. Proteins that relay a signal are most commonly phosphorylated at one or more sites, activating or inactivating the protein. Kinases catalyze...
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A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo
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Signaling Pathways Underlying Anthracycline Cardiotoxicity.

Valentina Sala1, Angela Della Sala1, Emilio Hirsch1

  • 1Department of Molecular Biotechnology and Health Sciences, University of Torino, Torino, Italy.

Antioxidants & Redox Signaling
|January 29, 2020
PubMed
Summary

Anthracyclines (ANTs) used in cancer treatment can cause severe cardiac side effects in survivors. Understanding ANTs cardiotoxicity mechanisms is crucial for developing effective prevention and treatment strategies.

Keywords:
DNA damageanthracyclinesautophagycalcium homeostasiscardiotoxicityreactive oxygen species

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Area of Science:

  • Cardiology
  • Oncology
  • Molecular Biology

Background:

  • Cardiac side effects of hematological treatments pose a significant threat to cancer survivors' survival.
  • Anthracyclines (ANTs) are potent antitumor agents but are highly cardiotoxic.
  • Current diagnosis, prevention, and treatment of ANTs-induced cardiotoxicity remain unmet clinical needs.

Purpose of the Study:

  • To review recent findings on the molecular mechanisms underlying anthracyclines (ANTs) cardiotoxicity.
  • To highlight the role of reactive oxygen species and signaling pathways in ANTs cardiotoxicity.
  • To discuss potential therapeutic targets and the need for clinical validation.

Main Methods:

  • Literature review of recent findings on ANTs cardiotoxicity.
  • Discussion of molecular pathways including DNA damage, mitochondrial dysfunction, calcium homeostasis, autophagy, and apoptosis.
  • Emphasis on reactive oxygen species and signaling pathway interactions.

Main Results:

  • ANTs cardiotoxicity involves complex molecular mechanisms including DNA and mitochondrial damage.
  • Disruptions in calcium homeostasis, autophagy, and apoptosis contribute to cardiac pathology.
  • Reactive oxygen species play a critical role, interacting with major signaling pathways.

Conclusions:

  • A deeper understanding of ANTs cardiotoxicity mechanisms is essential for clinical advancement.
  • New therapeutic targets and drugs show promise but require clinical validation.
  • Future research should focus on clinically relevant models for target validation.