CardioT Cancer Research Results

CardioT, Cardiotoxicity: Click to Expand ⟱
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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⟱
1780- MEL,    Utilizing Melatonin to Alleviate Side Effects of Chemotherapy: A Potentially Good Partner for Treating Cancer with Ageing
- Review, Var, NA
*antiOx↑, Melatonin is a potent antioxidant and antiageing molecule, is nontoxic, and enhances the efficacy and reduces the side effects of chemotherapy.
*toxicity↓,
ChemoSen↑,
*eff↑, melatonin was superior in preventing free radical destruction compared to other antioxidants, vitamin E, β-carotene, vitamin C, and garlic oil
*mitResp↑, increasing the expression and activity of the mitochondrial respiration chain complexes
*ATP↑, increasing the expression and activity of the mitochondrial respiration chain complexes
*ROS↓, most attractive property of melatonin is that its metabolites also regulate the mitochondrial redox status by scavenging ROS and RNS
*CardioT↓, melatonin has a protective effect on the heart without affecting DOX's antitumor activity,
*GSH↑, improving the de novo synthesis of glutathione (GSH) by promoting the activity of gamma-glutamylcysteine synthetase
*NOS2↓, melatonin inhibits the production of nitric oxide synthase (NOS)
*lipid-P↓, lipid peroxidation was reduced after melatonin treatment (role in induces organ failure)
eff↑, but it also enhances its antitumor activity more than vitamin E
*HO-1↑, melatonin upregulates heme oxygenase-1 (HO-1) (role in induces organ failure)
*NRF2↑, decreased bladder injury and apoptosis due to the upregulation of Nrf2 and nuclear transcription factor NF-κB expression
*NF-kB↑,
TumCP↓, significantly reduced cell proliferation
eff↑, Pretreatment with melatonin effectively preserved the ovaries from cisplatin-induced injury
neuroP↑, Melatonin has neuroprotective roles in oxaliplatin-induced peripheral neuropathy

1748- RosA,    The Role of Rosmarinic Acid in Cancer Prevention and Therapy: Mechanisms of Antioxidant and Anticancer Activity
- Review, Var, NA
AntiCan↑, RA exhibits significant potential as a natural agent for cancer prevention and treatment
*BioAv↝, Various factors, including its lipophilic nature, stability in the gastrointestinal tract, and interactions with food, can significantly influence its absorption
*CardioT↓, RA attenuated these effects by reducing ROS levels, indicating its potential role as a cardioprotective agent during chemotherapy.
*Iron↓, Another significant mechanism antioxidant activity of RA is its capacity to chelate transition metal ions, particularly iron (Fe2+) and copper (Cu2+), which can catalyze the formation of highly reactive hydroxyl radicals through the Fenton reaction.
*ROS↓, forming stable complexes with Fe2+ and Cu2+, thus inhibiting their pro-oxidant activity.
*SOD↑, SOD, CAT, and GPx, play crucial roles in neutralizing ROS and maintaining cellular redox homeostasis. RA upregulates the expression and activity of these enzymes
*Catalase↑,
*GPx↑,
*NRF2↑, activation of the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway, a primary regulator of the antioxidant response
MARK4↓, Anwar’s study demonstrated that RA inhibited MARK4 activity in MDA-MB-231 breast cancer cells, resulting in dose-dependent apoptosis
MMP9↓, RA effectively inhibited cancer cell invasion and migration by reducing matrix metalloproteinase-9 (MMP-9) activity
TumCCA↑, caused cell cycle arrest
Bcl-2↓, RA downregulates Bcl-2 expression and upregulates Bax, thereby promoting apoptosis
BAX↑,
Apoptosis↑,
E-cadherin↑, promoting E-cadherin expression, while downregulating N-cadherin and vimentin
N-cadherin↓,
Vim↓,
Gli1↓, induced apoptosis by downregulating Gli1, a key component of the Hedgehog signaling pathway,
HDAC2↓, RA induced apoptosis by modulating histone deacetylase 2 (HDAC2) expression
Warburg↓, anti-Warburg effect of RA in colorectal carcinoma
Hif1a↓, RA inhibits hypoxia-inducible factor-1 alpha (HIF-1α) and downregulates miR-155
miR-155↓,
p‑PI3K↑, RA has been shown to upregulate p-PI3K, protecting cells through the PI3K/Akt pathway,
ROS↑, RA, induces significant ROS generation in A549 cells, which triggers both apoptosis and autophagy.
*IronCh↑, RA’s dual nature as both a phenolic acid and a flavonoid-related compound enables it to chelate metal ions and prevent the formation of free radicals,

1747- RosA,    Molecular Pathways of Rosmarinic Acid Anticancer Activity in Triple-Negative Breast Cancer Cells: A Literature Review
- Review, BC, MDA-MB-231 - Review, BC, MDA-MB-468
TumCCA↑, Rosmarinic Acid arrests the G0/G1 phase in MDA-MB-231 cells and the S-phase in MDA-MB-468 cells following apoptosis (interruption of the G2/M process).
TNF-α↑, Rosmarinic Acid enhanced the expression of TNF (tumor necrosis factor), GADD45A (growth arrest and DNA damage-inducible 45 alpha), and the proapoptotic BNIP3
GADD45A↑,
BNIP3↑,
survivin↓, IRC5 (Survivin) inhibition appears to be the most important effect of Rosmarinic Acid on MDA-MB-468 cells
Bcl-2↓, Bcl-2 gene is downregulated while the Bax gene expression is increased in the presence of Rosmarinic Acid
BAX↑,
HH↓, The experiments showed that Rosmarinic Acid inhibited Hh signaling genes’ expression in BCSCs.
eff↑, rosemary extract with Rosmarinic Acid and carnosic acid as primary ingredients inhibited cancer cell viability in the ER+, HER2+, and TNBC subtypes (MDA-MB-231 and MDA-MB-468 cells)
ChemoSen↑, The inhibition of NF-κB increases chemotherapy and radiation results
RadioS↑,
TumCP↓, In vitro experiments in MDA-MB-231 cancer cells treated with Rosmarinic Acid have shown that proliferation and migration were significantly attenuated, and eventually, cells were led to apoptosis
TumCMig↓,
Apoptosis↑,
RenoP↑, Rosmarinic Acid decreased the hepatic and renal toxicity induced by methotrexate, as well as the cardiotoxicity of doxorubicin
CardioT↓,

1744- RosA,    Therapeutic Applications of Rosmarinic Acid in Cancer-Chemotherapy-Associated Resistance and Toxicity
- Review, Var, NA
chemoR↓, Recently, several studies have shown that RA is able to reverse cancer resistance to first-line chemotherapeutics
ChemoSideEff↓, as well as play a protective role against toxicity induced by chemotherapy and radiotherapy
RadioS↑, RA decreased radiation-induced ROS with RA by 21% compared to control
ROS↓, mainly due to its scavenger capacity
ChemoSen↑, recent years, evidence has emerged demonstrating the ability of RA to act as a chemosensitizer
BioAv↑, bioavailability of RA have been studied in animal models, revealing rapid absorption in the stomach and intestine
Half-Life↝, Urine was the primary route of RA excretion, with 83% of the total metabolites excreted during the period from 8 to 18 h after RA administration
antiOx↑, RA, well known for its antioxidant properties,
ROS↑, has recently been identified as a potential pro-oxidant in the presence of superoxide anions.
Fenton↑, Studies indicate that RA can facilitate the reduction of Cu (II) to Cu (I) and Fe (III) to Fe (II) leading to Fenton-type reactions that generate reactive hydroxyl radicals (HO˙)
DNAdam↑, These radicals are implicated in DNA damage and induction of apoptosis in cancer cells
Apoptosis↑,
CSCs↓, RA has demonstrated potential in controlling breast cancer stem cells (CSCs)
HH↓, RA inhibits stem-like breast cancer cells by targeting the hedgehog signaling pathway and modulating the Bcl-2/Bax ratio at concentrations of 270 and 810 μM
Bax:Bcl2↑,
MDR1↓, It has been observed to downregulate P-glycoprotein (P-gp) expression and decrease MDR1 gene transcription, thereby reversing MDR.
P-gp↓,
eff↑, RA has been reported to modulate the ADAM17/EGFR/AKT/GSK3β signaling axis in A375 melanoma cells, potentially enhancing synergy with cisplatin
eff↑, RA has demonstrated effectiveness in enhancing chemosensitivity to 5-FU, a commonly used chemotherapy agent for gastrointestinal cancers.
FOXO4↑, By upregulating FOXO4 expression, RA restored the sensitivity of cells to 5-FU
*eff↑, RA has been shown to reduce DOX-induced apoptosis in H9c2 cardiac muscle cells, and reduce intracellular ROS generation through downregulation of c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK), as well as to restore the
*ROS↓,
*JNK↓,
*ERK↓,
*GSH↑, RA has also shown an antioxidant role, which is evidenced by the ability and recovery of levels of glutathione (GSH), hydrogen peroxide (H2O2), and superoxide radicals (O2·), reducing the expression of malondialdehyde
*H2O2↑,
*MDA↓,
*SOD↑, regulating the expression of antioxidant enzymes such as superoxide dismutase (SOD), as well as upregulating catalase heme oxygenase-1, resulting in significantly improved viability
*HO-1↑,
*CardioT↓, The cardioprotective effect of RA
selectivity↑, RA blocked caspases 3 and 9 activation, cytochrome c release, and ROS generation induced by cisplatin in HEI-OC1(normal)cells

1495- SFN,  doxoR,    Sulforaphane protection against the development of doxorubicin-induced chronic heart failure is associated with Nrf2 Upregulation
- in-vivo, Nor, NA
*CardioT↓, SFN significantly prevented DOX-induced progressive cardiac dysfunction between 2-6 weeks and prevented DOX-induced cardiac function deterioration.
*NRF2↑, SFN upregulated NF-E2-related factor 2 (Nrf2)
*eff↓, protective effect of SFN against DOX-induced fibrotic and inflammatory responses was abolished by Nrf2 silencing.
*ROS↓, prevented DOX-induced cardiac oxidative stress

1494- SFN,  doxoR,    Sulforaphane potentiates anticancer effects of doxorubicin and attenuates its cardiotoxicity in a breast cancer model
- in-vivo, BC, NA - in-vitro, BC, MCF-7 - in-vitro, Nor, MCF10
CardioT↓, SFN (4 mg/kg, 5 days/week) protected against mortality and cardiac dysfunction induced by DOX
*GSH↑, Rats Hearts: SFN and DOX co-treatment reduced MDA and 4-HNE adduct formation and also prevented DOX-induced depletion of GSH levels
*ROS↓, SFN reduces DOX-induced oxidative stress in the heart of non-tumor bearing rats.
*NRF2↑, activates Nrf2 in rat hearts during DOX treatment
NRF2∅, SFN does not interfere with DOX toxicity or Nrf2 activity in breast cancer cell lines
HDAC↓, SFN acts synergistically with DOX to inhibit HDAC and DNMT activity, decrease ERα detection and increase caspase-3 activity
DNMTs↓,
Casp3↑,
ER-α36↓, ERα levels in MCF-7, MDA-MB-231
Remission↑, SFN+DOX treatment (with a total DOX dose of 20 mg/kg) was able to eradicate the tumors in all rats by day 35 after tumor implantation
eff↑, SFN (4 mg/kg oral; 5 days/week for 5 weeks) with DOX (total of 10 or 20 mg/kg i.p. administered over 4 weeks) and showed that in combination with SFN, the dosage of DOX could be < by 50% while still eliciting the same anti-cancer effects as DOX alone
ROS↑, Increased generation of reactive oxygen species (ROS), an altered redox status, and aerobic glycolysis for energy production distinguish highly proliferative cancer cells from normal healthy cells
selectivity?, ROS production... distinguish highly proliferative cancer cells from normal healthy cells

1484- SFN,    Sulforaphane’s Multifaceted Potential: From Neuroprotection to Anticancer Action
- Review, Var, NA - Review, AD, NA
neuroP↑, current evidence supporting the neuroprotective and anticancer effects of SFN
AntiCan↑,
NRF2↑, neuroprotective effects through the activation of the Nrf2 pathway
HDAC↓, histone deacetylase was inhibited after human subjects ingested 68 g of broccoli sprouts
eff↑, sensitize cancer cells to chemotherapy
*ROS↓, protecting neurons [14] and microglia [15] against oxidative stress
neuroP↑, neuroprotective effects in Alzheimer’s disease (AD)
HDAC↓, capacity as a histone deacetylase (HDAC) inhibitor
*toxicity∅, normal cells are relatively resistant to SFN-induced cell death
BioAv↑, SFN has good bioavailability; it can reach high intracellular and plasma concentrations
eff↓, However, it is important to consider that at lower doses, specifically 2.5 μM, SFN resulted in a slight increase in cell proliferation by 5.18–11.84% within a 6 to 48 h treatment window
cycD1/CCND1↓, in breast cancer
CDK4↓, in breast cancer
p‑RB1↓, in breast cancer
Glycolysis↓, in prostate cancer
miR-30a-5p↑, ovarian cancer
TumCCA↑, gastric cancer
TumCG↓,
TumMeta↓,
eff↑, SFN emerged as a critical enhancer of ST’s efficacy by suppressing resistance in RCC cells, offering a potent approach to overcome ST monotherapy limitations.
ChemoSen↑, SFN may improve the effectiveness of chemotherapy by increasing cancer cell sensitivity to the drugs used to treat them
RadioS↑, SFN may help protect healthy cells and tissues from the harmful effects of radiation
CardioT↓, Several studies have demonstrated the protective role of SFN in cardiotoxicity
angioG↓, In colon cancers, SFN blocks cells’ progression and angiogenesis by inhibiting HIF-1α and VEGF expression
Hif1a↓,
VEGF↓,
*BioAv?, SFN is well absorbed in the intestine, with an absolute bioavailability of approximately 82%.
*Half-Life∅, In rats, after an oral dose of 50 μmol of SFN, the plasma concentration of SFN can peak at 20 μM at 4 h and decline with a half-life of about 2.2 h


Showing Research Papers: 1 to 7 of 7

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Fenton↑, 1,   NRF2↑, 1,   NRF2∅, 1,   ROS↓, 1,   ROS↑, 3,  

Core Metabolism/Glycolysis ⓘ

Glycolysis↓, 1,   Warburg↓, 1,  

Cell Death ⓘ

Apoptosis↑, 3,   BAX↑, 2,   Bax:Bcl2↑, 1,   Bcl-2↓, 2,   Casp3↑, 1,   survivin↓, 1,  

Transcription & Epigenetics ⓘ

miR-30a-5p↑, 1,  

Autophagy & Lysosomes ⓘ

BNIP3↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   DNMTs↓, 1,   GADD45A↑, 1,  

Cell Cycle & Senescence ⓘ

CDK4↓, 1,   cycD1/CCND1↓, 1,   p‑RB1↓, 1,   TumCCA↑, 3,  

Proliferation, Differentiation & Cell State ⓘ

CSCs↓, 1,   FOXO4↑, 1,   Gli1↓, 1,   HDAC↓, 3,   HDAC2↓, 1,   HH↓, 2,   p‑PI3K↑, 1,   TumCG↓, 1,  

Migration ⓘ

E-cadherin↑, 1,   ER-α36↓, 1,   MARK4↓, 1,   miR-155↓, 1,   MMP9↓, 1,   N-cadherin↓, 1,   TumCMig↓, 1,   TumCP↓, 2,   TumMeta↓, 1,   Vim↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   Hif1a↓, 2,   VEGF↓, 1,  

Barriers & Transport ⓘ

P-gp↓, 1,  

Immune & Inflammatory Signaling ⓘ

TNF-α↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 2,   chemoR↓, 1,   ChemoSen↑, 4,   eff↓, 1,   eff↑, 8,   Half-Life↝, 1,   MDR1↓, 1,   RadioS↑, 3,   selectivity?, 1,   selectivity↑, 1,  

Functional Outcomes ⓘ

AntiCan↑, 2,   CardioT↓, 3,   ChemoSideEff↓, 1,   neuroP↑, 3,   Remission↑, 1,   RenoP↑, 1,  
Total Targets: 62

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↑, 1,   GPx↑, 1,   GSH↑, 3,   H2O2↑, 1,   HO-1↑, 2,   Iron↓, 1,   lipid-P↓, 1,   MDA↓, 1,   NRF2↑, 4,   ROS↓, 6,   SOD↑, 2,  

Metal & Cofactor Biology ⓘ

IronCh↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↑, 1,   mitResp↑, 1,  

Cell Death ⓘ

JNK↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↓, 1,  

Immune & Inflammatory Signaling ⓘ

NF-kB↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv?, 1,   BioAv↝, 1,   eff↓, 1,   eff↑, 2,   Half-Life∅, 1,  

Clinical Biomarkers ⓘ

NOS2↓, 1,  

Functional Outcomes ⓘ

CardioT↓, 4,   toxicity↓, 1,   toxicity∅, 1,  
Total Targets: 27

Scientific Paper Hit Count for: CardioT, Cardiotoxicity
3 Rosmarinic acid
3 Sulforaphane (mainly Broccoli)
2 doxorubicin
1 Melatonin
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

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