Fibrosis Cancer Research Results

Fibrosis, Fibrosis: Click to Expand ⟱
Source: HalifaxProj(inhibit)
Type:
Causes tissue to overgrow, harden, and scar due to chronic inflammation Chronic fibrosis can create an environment conducive to cancer development. For example, in liver cirrhosis (a form of fibrosis), there is an increased risk of liver cancer (hepatocellular carcinoma). Similarly, pulmonary fibrosis has been associated with an increased risk of lung cancer.

Fibrosis plays a significant role in cancer biology, influencing tumor progression, metastasis, and treatment response. The fibrotic microenvironment can create conditions that support tumor growth and resistance to therapies, often correlating with poor prognosis across various cancer types.
Scientific Papers found: Click to Expand⟱
1206- Caff,    Caffeine inhibits TGFβ activation in epithelial cells, interrupts fibroblast responses to TGFβ, and reduces established fibrosis in ex vivo precision-cut lung slices
- in-vitro, NA, NA - ex-vivo, NA, NA
Fibrosis↓,
TGF-β↓, inhibited TGFβ activation by lung epithelial cells in a concentration-dependent manner but had no effect on TGFβ activation in fibroblasts.
α-SMA↓,

7012- Fuc,    Fucoidan: A promising natural therapeutic agent for protecting human kidney health
- Review, EC, NA
*RenoP↑, Fucoidan exhibits significant anti-inflammatory effects in kidney protection.
*Inflam↓,
*antiOx↑, Antioxidant properties effectively reduce oxidative stress in renal tissues.
*ROS↓,
*BloodF↑, Enhances renal function by improving blood flow and diuresis.
*diuretic↑,
*BioAv↓, High-MW fucoidans often display stronger anticoagulant and viscosity-modulating effects. However, they may have limited oral bioavailability,
*BioAv↑, whereas low- to medium-MW fractions show improved tissue penetration, more favorable absorption, and can retain potent anti-inflammatory and anti-fibrotic activities, making them attractive for chronic kidney disease applications
*MAPK↓, (LMWF) has been reported in models of renal ischemia-reperfusion injury, where it inhibits the MAPK signaling pathway and subsequently reduces inflammation and fibrosis
*ERK↑, fucoidan can activate the ERK/MAPK signaling pathway, which plays a crucial role in preserving the endothelial glycocalyx in CKD
*NLRP3↓, fucoidan attenuates NLRP3 inflammasome activation and subsequent podocyte pyroptosis, ultimately leading to improved renal function and reduced inflammation in diabetic kidney disease (DKD)
*NRF2↑, By inhibiting ROS-generating systems (e.g., NADPH oxidase) and activating Nrf2-dependent transcription of antioxidant genes, fucoidan limits mitochondrial dysfunction and prevents oxidative injury to podocytes and tubular epithelial cells
*MDA↓, fucoidan nanoparticles significantly reduced levels of malondialdehyde (MDA), a marker of lipid peroxidation and oxidative stress, while simultaneously upregulating the levels of superoxide dismutase (SOD) and glutathione peroxidase (GPx)
*SOD↑,
*GPx↑,
*Catalase↑, Altogether, fucoidan directly reduces renal oxidative stress by scavenging reactive oxygen species and upregulating endogenous antioxidant defenses (e.g., SOD, CAT, GPx) in tubular and glomerular cells, by suppressing upstream ROS generation
*lipid-P↓, fucoidan limits lipid peroxidation and DNA damage, thereby preserving podocyte integrity and tubular epithelial viability
*DNAdam↓,
*Fibrosis↓, Inhibition of fibrosis
*JAK2↓, fucoidan combats renal fibrosis is via the restriction of the JAK2/STAT3 signaling pathway.
*STAT3↓,
*uricA↓, By reducing serum uric acid levels, fucoidan significantly inhibits the activation of JAK2/STAT3, consequently decreasing the expression of key fibrotic markers such as collagen I and α-smooth muscle actin (α-SMA)
*COL1↓,
*α-SMA↓,
*SIRT1↑, fucoidan’s anti-fibrotic effects are further attributed to its activation of protective pathways such as Sirt-1, GLP-1R, and Nrf2/HO-1(
*HO-1↑,
*GLP-1R↑,
*HMGB1↓, Stimulating these protective pathways results in the inhibition of pro-fibrotic signaling cascades, including the HMGB1/RAGE/NF-κB/TGF-β1 pathway
*RAGE↓,
*NF-kB↓,
*TGF-β1↓,
*PI3K↓, Fucoidan also exhibits potential in curtailing the inflammatory processes associated with renal fibrosis through its inhibitory effects on the PI3K/Akt/NF-κB signaling cascade.
*Akt↓,
*GutMicro↑, research has elucidated the important role of gut microbiota in mediating the protective effects of fucoidan, suggesting that modulation of microbial communities may underlie its benefits in renal health
*SCFAs↑, Fucoidan’s positive impact on gut microbiota includes enhancing the production of short-chain fatty acids (SCFAs), especially butyrate, which are known to support gut integrity and overall health (
*Buty↑,
*IBI↑, Fucoidan's ability to enhance SCFA production has been linked to improved intestinal barrier integrity, a crucial factor in preventing the translocation of harmful substances into the bloodstream, which can exacerbate kidney injury
*TJ↑, Studies indicate that fucoidan can upregulate the expression of tight junction proteins, crucial for maintaining the integrity of the intestinal epithelium
*Dose↝, national approval in China for renal indications, indicate that fucoidan is generally safe at oral doses of 50–300 mg/day and up to 1–3 g/day in short‑ to mid‑term studies, with no major hematologic, hepatic, or renal toxicity reported.


Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


Migration(tgid=13) ⓘ

Fibrosis↓, 1,   TGF-β↓, 1,   α-SMA↓, 1,  
Total Targets: 3

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

Buty↑, 1,   diuretic↑, 1,   GLP-1R↑, 1,   SCFAs↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 1,   Catalase↑, 1,   GPx↑, 1,   HO-1↑, 1,   lipid-P↓, 1,   MDA↓, 1,   NRF2↑, 1,   ROS↓, 1,   SOD↑, 1,   uricA↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

SIRT1↑, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   MAPK↓, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↓, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

ERK↑, 1,   PI3K↓, 1,   STAT3↓, 1,  

Migration(tgid=13) ⓘ

COL1↓, 1,   Fibrosis↓, 1,   RAGE↓, 1,   TGF-β1↓, 1,   TJ↑, 1,   α-SMA↓, 1,  

Barriers & Transport(tgid=15) ⓘ

IBI↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

HMGB1↓, 1,   Inflam↓, 1,   JAK2↓, 1,   NF-kB↓, 1,  

Protein Aggregation(tgid=19) ⓘ

NLRP3↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   BioAv↑, 1,   Dose↝, 1,  

Clinical Biomarkers(tgid=22) ⓘ

BloodF↑, 1,   GutMicro↑, 1,   RAGE↓, 1,  

Functional Outcomes(tgid=23) ⓘ

RenoP↑, 1,  
Total Targets: 40

Scientific Paper Hit Count for: Fibrosis, Fibrosis
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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