CardioT Cancer Research Results

CardioT, Cardiotoxicity: Click to Expand ⟱
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Type:
Cardiotoxicity in the context of cancer generally refers to the potential harmful effects that cancer therapies can have on the heart. This is an important consideration because many effective cancer treatments can also damage cardiac tissue, leading to short-term or long-term cardiovascular complications.

Mechanisms of Cardiotoxicity in Cancer Therapy
-Chemotherapy Agents:
     Anthracyclines (e.g., doxorubicin, epirubicin):
     Alkylating Agents (e.g., cyclophosphamide):
     Antimetabolites (e.g., 5-fluorouracil, capecitabine):
-Targeted Therapies:
    HER2 inhibitors (e.g., trastuzumab):
    Tyrosine Kinase Inhibitors (e.g., sunitinib, imatinib):
-Radiation Therapy:
    Thoracic irradiation:

Natural Products that may reduce Cardiotoxicity:
-Resveratrol
-Curcumin
-EGCG
-Quercetin
-Garlic Extract (Allicin)
-Omega-3 Fatty Acids: Fish oil (EPA and DHA), flaxseeds, chia seeds, walnuts.


Natural products like resveratrol, curcumin, EGCG, quercetin, garlic extract, and omega-3 fatty acids show potential in reducing cardiotoxicity by targeting oxidative stress, inflammation, and apoptotic pathways.
Scientific Papers found: Click to Expand⟱
5964- CEL,    Celecoxib pathways: pharmacokinetics and pharmacodynamics
- Review, Var, NA
COX2↓, purposefully designed as COX-2-selective inhibitors
*Pain↓, one of the most frequently prescribed drugs for the relief of pain and inflammation
*Inflam↓,
Apoptosis↑, proposed anticarcinogenic mechanisms of celecoxib include induction of apoptosis, cell cycle arrest, regulation of angiogenesis, and induction of endoplasmic reticulum (ER) stress.
TumCCA↑,
angioG↓,
ER Stress↑,
VEGF↓, Celecoxib treatment decreased the expression of vascular endothelial cell growth factor [53-55] and inhibition of matrix metalloproteinase 9
MMP9↓,
PDK1↓, inhibition of PDK1/Akt signaling correlated with celecoxib-induced apoptosis in both colon and prostate tumor cell lines [
Akt↓,
CA↓, Carbonic anhydrases (CA), enzymes that catalyze the reversible hydration of carbon dioxide, are also inhibited by celecoxib (IC50 in the low nanomolar range)
CardioT↑, selective COX-2 inhibitors, rofecoxib, valdecoxib, and celecoxib with an increased incidence of myocardial infarction, stroke, and death due to cardiovascular causes

5960- CEL,    Phase II, Randomized, Placebo-Controlled Trial of Neoadjuvant Celecoxib in Men With Clinically Localized Prostate Cancer: Evaluation of Drug-Specific Biomarkers
- Trial, Pca, NA
eff∅, Treatment with 4 to 6 weeks of celecoxib had no effect on intermediate biomarkers of prostate carcinogenesis, despite the achievement of measurable tissue levels.
Dose↝, We caution against using celecoxib 400 mg twice daily as a preventive agent for prostate cancer in additional studies.
CardioT↑, The potential benefits of celecoxib in patients with prostate cancer should be weighed against the possible increase of cardiovascular toxicities linked to this agent.

5948- Cela,    Recent Trends in anti-tumor mechanisms and molecular targets of celastrol
TumCP↓, mechanism of action of celastrol in terms of inhibition of cell proliferation and regulation of the cell cycle, regulation of apoptosis and autophagy, inhibition of cell invasion and metastasis, anti-inflammation, regulation of immunotherapy, and an
TumCCA↑,
Apoptosis↑,
TumAuto↑,
TumCI↓,
TumMeta↓,
Imm↝,
angioG↓,
Cyt‑c↑, release of cytochrome c (CytC)
ROS↑, increasing ROS levels, and activating the mitochondrial apoptosis pathway
BAX↑, upregulating the expression of CytC and the pro-apoptotic protein Bax, activating caspase-3 and caspase-9, and leading to the cleavage of PARP
Casp3↑,
Casp9↑,
cl‑PARP↑,
PrxII↓, binds to peroxiredoxin-2 (Prdx2) and inhibits its enzyme activity,
ER Stress↑, resulting in ROS-dependent endoplasmic reticulum (ER) stress, mitochondrial dysfunction, and apoptosis in gastric cancer cells
mtDam↑,
CHOP↑, celastrol upregulates the expression of CHOP, Bip, XBP1s, and IRE1 proteins,
Inflam↓, Anti-inflammatory properties of celastrol
NF-kB↓, Celastrol additionally obstructed NF-κB and its downstream gene products, such as CXCR4 and MMP9, and reduced serum IL-6 and TNF-α levels to inhibit cell invasion and migration in vivo
CXCR4↓,
MMP9↓,
IL6↓,
TNF-α↓,
HSP90↓, accumulation may be due to the inhibition of HSP90 and the stress response
neuroP↑, Our mass spectrometry research also showed that celastrol directly binds to HSP90 and HSP70, exerting antitumor and neuroprotective effects
STAT3↓, Celastrol exerts anti-tumor activity by inhibiting STAT3
Prx↓, celastrol binds directly to Prdx1, Prdx2, Prdx4, and Prdx6 via active cysteine sites, inhibiting their antioxidant activity without affecting protein expression
HO-1↑, Celastrol also targeted heme oxygenase-1 (HO-1), increasing its expression in activated hematopoietic stem cells
eff↑, Research has indicated that celastrol, combined with 17-N-Allylamino-17-demethoxygeldanamycin (17-AAG), inhibits the toxic stress response of HSP90-targeted proteins, reduces the sensitization of human glioblastomas to celastrol treatment, an
eff↑, celastrol, when combined with EGFR tyrosine kinase inhibitors (EGFR-TKIs), effectively inhibits the growth and invasion of T790M mutant human lung cancer H1975
BioAv↑, nano-delivery systems present a novel pathway for the development and clinical application of celastrol, potentially overcoming existing limitations and maximizing its therapeutic potential.
toxicity↑, several significant challenges, including its pronounced hepatic and renal toxicity and potential for causing immunosuppression
CardioT↑, celastrol, which includes hepatotoxicity, cardiotoxicity, infertility toxicity, hematopoietic system toxicity and nephrotoxicity.
hepatoP↓,


Showing Research Papers: 1 to 3 of 3

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

HO-1↑, 1,   Prx↓, 1,   PrxII↓, 1,   ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

mtDam↑, 1,  

Core Metabolism/Glycolysis ⓘ

PDK1↓, 1,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis↑, 2,   BAX↑, 1,   Casp3↑, 1,   Casp9↑, 1,   Cyt‑c↑, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   ER Stress↑, 2,   HSP90↓, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 1,  

DNA Damage & Repair ⓘ

cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

TumCCA↑, 2,  

Proliferation, Differentiation & Cell State ⓘ

STAT3↓, 1,  

Migration ⓘ

CA↓, 1,   MMP9↓, 2,   TumCI↓, 1,   TumCP↓, 1,   TumMeta↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 2,   VEGF↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   CXCR4↓, 1,   IL6↓, 1,   Imm↝, 1,   Inflam↓, 1,   NF-kB↓, 1,   TNF-α↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   Dose↝, 1,   eff↑, 2,   eff∅, 1,  

Clinical Biomarkers ⓘ

IL6↓, 1,  

Functional Outcomes ⓘ

CardioT↑, 3,   hepatoP↓, 1,   neuroP↑, 1,   toxicity↑, 1,  
Total Targets: 42

Pathway results for Effect on Normal Cells:


Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  

Functional Outcomes ⓘ

Pain↓, 1,  
Total Targets: 2

Scientific Paper Hit Count for: CardioT, Cardiotoxicity
2 Celecoxib
1 Celastrol
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:1108  State#:%  Dir#:2
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