necrosis Cancer Research Results
necrosis, necrosis: Click to Expand ⟱
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| Type: type of cell death |
Necrosis is a type of cell death that occurs when cells are damaged or injured, leading to the loss of cellular homeostasis and the eventual death of the cell. Necrosis is a non-programmed form of cell death, meaning that it is not a deliberate or controlled process, but rather a response to cellular damage or injury.
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Scientific Papers found: Click to Expand⟱
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Review, |
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Stroke, |
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Diabetic, |
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*antiOx↑, *AntiCan↑, *AntiDiabetic↑, *cardioP↑, *Obesity↓, *hepatoP↑, *AntiAg↑, *Bacteria↓, *Imm↑, MMP2↓, MMP9↓, Apoptosis↓, MMP↓, ERK↓, PI3K↓, ALAT↓, *ROS↓, *Catalase↑, *SOD↑, *GPx↑, *AST↓, *LDH↓, *necrosis↓, ROS↑, TumCCA↑, CDK4↓, cycD1/CCND1↓, NOTCH↓, IL6↓, chemoP↑, *Pain↓, *neuroP↑, *TRPM7↓, *motorD↑, *NF-kB↓, *COX2↓, *MDA↓,
*other↑, *necrosis↓, *IL6↑, *TGF-β↑, *iNOS↑, *MMP2↑, *MCP1↑, *HO-1↑, *Inflam↓, *IL1β↓, *IL6↓, *TNF-α↓, *BioAv↑, eff⇅, DNAdam↑, Apoptosis↑, ROS↑, TumCP↓, *ROS↓, *FGF↑,
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AD, |
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Park, |
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*neuroP↑, *ROS↓, *Inflam↓, *Apoptosis↓, *BBB?, *tau↓, *NF-kB↓, *IL1β↓, *TNF-α↓, *IL4↓, *MAPK↓, *memory↑, *cognitive↑, *Aβ↓, *ROS↓, *lipid-P↓, *GSH↑, *MDA↓, *SOD↑, *Catalase↑, *AChE↓, *BChE↓, *p‑ERK↓, *p‑JNK↓, *p‑p38↓, *GutMicro↑, *COX2↓, *iNOS↓, *TLR4↓, *neuroP↑, *Strength↑, *AMPK↑, *MMP↑, *necrosis↓, *NRF2↑, *HO-1↑,
*antiOx↑, *Inflam↓, *lipid-P↓, *necrosis↓, *hepatoP↑, *IL1↓, *IL6↓, *TNF-α↓, *IFN-γ↓, MAPK↓, Apoptosis↑, Cyt‑c↑, Casp3↑, Casp9↑, *PPARγ↑, *GLUT4↑, *HSPs↓, *HSP27↑, *Trx↑, *SIRT1↑, *ALAT↓, *GSH↑, *lipid-P↓, *TNF-α↓, TumCG↓, P21↑, CDK4↑,
Showing Research Papers: 1 to 4 of 4
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 4
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
ROS↑, 2,
Mitochondria & Bioenergetics ⓘ
MMP↓, 1,
Core Metabolism/Glycolysis ⓘ
ALAT↓, 1,
Cell Death ⓘ
Apoptosis↓, 1, Apoptosis↑, 2, Casp3↑, 1, Casp9↑, 1, Cyt‑c↑, 1, MAPK↓, 1,
DNA Damage & Repair ⓘ
DNAdam↑, 1,
Cell Cycle & Senescence ⓘ
CDK4↓, 1, CDK4↑, 1, cycD1/CCND1↓, 1, P21↑, 1, TumCCA↑, 1,
Proliferation, Differentiation & Cell State ⓘ
ERK↓, 1, NOTCH↓, 1, PI3K↓, 1, TumCG↓, 1,
Migration ⓘ
MMP2↓, 1, MMP9↓, 1, TumCP↓, 1,
Immune & Inflammatory Signaling ⓘ
IL6↓, 1,
Drug Metabolism & Resistance ⓘ
eff⇅, 1,
Clinical Biomarkers ⓘ
ALAT↓, 1, IL6↓, 1,
Functional Outcomes ⓘ
chemoP↑, 1,
Total Targets: 27
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 2, Catalase↑, 2, GPx↑, 1, GSH↑, 2, HO-1↑, 2, lipid-P↓, 3, MDA↓, 2, NRF2↑, 1, ROS↓, 4, SOD↑, 2, Trx↑, 1,
Mitochondria & Bioenergetics ⓘ
MMP↑, 1,
Core Metabolism/Glycolysis ⓘ
ALAT↓, 1, AMPK↑, 1, LDH↓, 1, PPARγ↑, 1, SIRT1↑, 1,
Cell Death ⓘ
Apoptosis↓, 1, iNOS↓, 1, iNOS↑, 1, p‑JNK↓, 1, MAPK↓, 1, necrosis↓, 4, p‑p38↓, 1,
Transcription & Epigenetics ⓘ
other↑, 1,
Protein Folding & ER Stress ⓘ
HSP27↑, 1, HSPs↓, 1,
Proliferation, Differentiation & Cell State ⓘ
p‑ERK↓, 1, FGF↑, 1, TRPM7↓, 1,
Migration ⓘ
AntiAg↑, 1, MMP2↑, 1, TGF-β↑, 1,
Barriers & Transport ⓘ
BBB?, 1, GLUT4↑, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 2, IFN-γ↓, 1, IL1↓, 1, IL1β↓, 2, IL4↓, 1, IL6↓, 2, IL6↑, 1, Imm↑, 1, Inflam↓, 3, MCP1↑, 1, NF-kB↓, 2, TLR4↓, 1, TNF-α↓, 4,
Synaptic & Neurotransmission ⓘ
AChE↓, 1, BChE↓, 1, tau↓, 1,
Protein Aggregation ⓘ
Aβ↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↑, 1,
Clinical Biomarkers ⓘ
ALAT↓, 1, AST↓, 1, GutMicro↑, 1, IL6↓, 2, IL6↑, 1, LDH↓, 1,
Functional Outcomes ⓘ
AntiCan↑, 1, AntiDiabetic↑, 1, cardioP↑, 1, cognitive↑, 1, hepatoP↑, 2, memory↑, 1, motorD↑, 1, neuroP↑, 3, Obesity↓, 1, Pain↓, 1, Strength↑, 1,
Infection & Microbiome ⓘ
Bacteria↓, 1,
Total Targets: 71
Scientific Paper Hit Count for: necrosis, necrosis
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#:781 State#:% Dir#:1
wNotes=0 sortOrder:rid,rpid
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