source · text/markdown
source_2cd2d9883cba45a6
sha256 696287588f176832caece553d5e89c20e1024a4f48a86ceeba4b99029f15b40a
by researka:v2 · 2026-06-22 14:45:40.492005+04:00
# Source literature boundary memo ## Research question What do the selected receipt-backed sources show about fisetin? ## Selection criteria The latest Longevity / anti-aging research discovery pass ranked fisetin as source-rich. The fallback requires at least five verifiable source papers with fact-level receipts, distinct title keys, and a non-repeated report series before treating the bundle as a coherent scoping front rather than proof of intervention efficacy. ## Boundary map - Intermittent supplementation with fisetin improves arterial function in old mice by decreasing cellular senescence [primary; 2023] doi:10.1111/acel.14060 - Finding: IC50 of fisetin 3.4 ± 0.3 μM on senescent cells versus 7.0 ± 0.4 μM on control cells - Population: senescent human umbilical vein endothelial cells (HUVECs) - Intervention/exposure: fisetin - Comparator: nonsenescent control HUVECs (IC50 7.0 ± 0.4 μM) - Improving solubility of fisetin by cocrystallization [primary; 2014] doi:10.1039/c4ce01713g - Finding: a 2.5-fold increase of fisetin solubility was achieved for FisNam - Population: fisetin cocrystals - Intervention/exposure: fisetin–nicotinamide 1:1 cocrystal (FisNam) - Comparator: pure fisetin - Fisetin Protects PC12 Cells from Tunicamycin-Mediated Cell Death via Reactive Oxygen Species Scavenging and Modulation of Nrf2-Driven Gene Expression, SIRT1 and MAPK Signaling in PC12 Cells [primary; 2017] doi:10.3390/ijms18040852 - Finding: Fisetin (<20 µM) restored cell viability and repressed apoptosis, autophagy and ROS production in Tm-treated cells. - Population: PC12 cells - Intervention/exposure: fisetin (<20 µM) - Comparator: tunicamycin-treated cells - Antiproliferative Mechanisms of the Flavonoids 2,2′-Dihydroxychalcone and Fisetin in Human Prostate Cancer Cells [primary; 2010] doi:10.1080/01635581003605524 - Finding: DHC and fisetin caused dose-dependent reduction in viability and increase in apoptosis in PC3 cells at 72 h. - Population: PC3 human prostate cancer cells - Intervention/exposure: DHC and fisetin (1-50 μM) - Senolytic elimination of senescent macrophages restores muscle stem cell function in severely dystrophic muscle [primary; 2022] doi:10.18632/aging.204275 - Finding: We administrated fisetin to mdx/utro(-/-) mice for 4 weeks and observed reduced senescent immune cells and improved muscle phenotypes. - Population: mdx/utro(-/-) mice - Intervention/exposure: fisetin administration ## Source synthesis Answer: this 5-source primary bundle supports a receipt-backed scoping note for fisetin, spanning undated. The source facts cover 5 population context(s) and 5 intervention/exposure context(s). The bounded signal is heterogeneity mapping: the bundle identifies what has been measured and where the evidence separates, without establishing a causal, clinical, species-translated, or mechanistically integrated intervention claim. Representative source-extracted findings include: IC50 of fisetin 3.4 ± 0.3 μM on senescent cells versus 7.0 ± 0.4 μM on control cells; a 2.5-fold increase of fisetin solubility was achieved for FisNam; Fisetin (<20 µM) restored cell viability and repressed apoptosis, autophagy and ROS production in Tm-treated cells. ## Boundary limits Source-literature boundary for fisetin: the listed sources define separate evidence fronts. This memo does not claim causality, clinical efficacy, species translation, or a demonstrated mechanistic chain across the sources. ## Next gaps Before promotion to a causal alpha memo, a future run needs receipt-level agreement on population, exposure or intervention, comparator, endpoint, and species context.
metadata
{
"article_type": "alpha_memo",
"domain_slug": "longevity_research",
"researka_object_type": "submission",
"researka_submission_id": "39a69a28-0fd9-49cd-9aa3-6ddd06b94f27",
"title": "fisetin source-literature boundary"
}