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Open research questions in Genomics, phytochemicals, and oxidative stress

27 unresolved questions extracted from the limitations and future-work sections of 165 Genomics, phytochemicals, and oxidative stress papers in our library. Each links back to the study that raised it.

What the literature leaves open

  • Although experimental Scientific caution is necessary when linking cruciferous vegetables to the prevention of esophageal and isothiocyanates with many beneficial mechanisms, the exact amount in humans, duration of consumption, genetic polymorphisms, gut microbiota, and the role of cooking methods have not yet been fully determined.

    PREVENTION OF ESOPHAGEAL CANCER USING TRADITIONAL MEDICINE APPROACHES AND THE MECHANISM OF ACTION OF CRUCIFEROUS VEGETABLES · 2026 · DOI

  • Whether the observed stronger IGSL biosynthesis induction in response to C. higginsianum compared to abiotic stressors occurs through PAMP recognition or other pathogen-specific recognition mechanisms needs further elucidation.

    Response of the Arabidopsis indolic secondary metabolite network to infection with Colletotrichum higginsianum · 2026 · DOI

  • The hypothesis that IAN produced by myrosinase cleavage of IGSL provides a source of building blocks for camalexin biosynthesis and that conversion of IAN to GS-IAN occurs in the presence of GSH involving alternative P450 enzymes requires further experimental validation.

    Response of the Arabidopsis indolic secondary metabolite network to infection with Colletotrichum higginsianum · 2026 · DOI

  • The findings summarized in this review reveal that Nrf3 is not only the “youngest” member of the CNC bZIP family but also a multifaceted regulator of cellular homeostasis. Its ER-dependent maturation process, the proteolytic cleavages mediated by DDI2 or potentially NGLY1, the degradation cycle along the ERAD/SCF axis, and the stress-sensitive translocation steps remain incompletely mapped. Filling these biochemical gaps will be critical for understand- ing the tissue-specific functions of Nrf3. Evidence indi- cates that Nrf3 can exert a dual role in cancer: on the one hand, promoting proliferation, metabolic reprogramming, angiogenesis, and invasion through targets such as POMP, GLUT1, SREBP2-mevalonate, and VEGF; on the other hand, inhibiting oncogenic MAPK/ERK and AKT signal- ing axes, thereby reducing metastatic capacity and EMT in specific settings, such as certain breast and squamous cell carcinoma models. This “two-faced” effect likely intersects with tumor type-specific epigenetic landscapes, miRNA networks (e.g., miR-23b-3p, miR-99a-3p, miR-1246), and microenvironmental factors such as cytokine-Wnt-NF-κB signaling. Future studies should address (i) the promoter motifs to which Nrf3 displays high affinity in place of AREs, (ii) the mechanisms by which it regulates extracel- lular lipid uptake and macropinocytosis, and (iii) how it integrates ROS accumulation into differentiation decisions- approaches that will require advanced omics platforms and live-cell imaging models. Moreover, combination strategies involving small-molecule inhibitors targeting Nrf3, protea- some inhibitors, or mevalonate pathway blockers represent promising candidates for clinical translation in tumors with high therapeutic susceptibility, particularly pancreatic, hepatocellular, and thyroid cancers. Author contributions All authors reviewed the manuscript. Funding Open access funding provided by the Scientific and Tech- nological Research Council of Türkiye (TÜBİTAK). This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors. Data availability No datasets were generated or analysed during the current study.

    Nrf3: an emerging player in cancer, inflammation, and cellular homeostasis · 2026 · DOI

  • The Clark electrode-based mitochondrial respiration measurements were performed at a single 24-month timepoint; longitudinal assessment of mitochondrial respiratory capacity (Complexes I-IV, ATP synthase activity) at multiple intervals (baseline, 3, 6, 12, 24 months) during and after CTCT exposure would establish the temporal dynamics of mitochondrial impairment.

    Cardiotoxic Cancer Treatment (CTCT) Promotes Oxidative Stress and Alters Monocyte/ macrophage Biology · 2019 · DOI

  • Monocyte/macrophage biology alterations induced by cardiotoxic cancer treatment (CTCT) and their mechanistic link to oxidative stress-driven sarcopenia and cardiac dysfunction remain unexplored. Direct investigation of how CTCT-altered macrophage polarization (M1/M2 phenotypes) and inflammatory mediator production influence mitochondrial dysfunction in target tissues is needed.

    Cardiotoxic Cancer Treatment (CTCT) Promotes Oxidative Stress and Alters Monocyte/ macrophage Biology · 2019 · DOI

  • The study evaluated mitochondrial function exclusively in old female Wistar rat quadriceps after combined MTF + exercise treatment; the comparative efficacy of this intervention in cardiac tissue, male animals, and younger age groups requires investigation to establish generalizability across tissues and sexes.

    Cardiotoxic Cancer Treatment (CTCT) Promotes Oxidative Stress and Alters Monocyte/ macrophage Biology · 2019 · DOI

  • The benefits of combined metformin (MTF) + exercise treatment in preventing cardiotoxic cancer treatment (CTCT)-induced sarcopenia remain controversial and poorly characterized. Specifically, the mechanisms by which MTF + exercise synergistically preserve mitochondrial biogenesis, mitochondrial respiration, and mitochondrial replacement via mitophagy in CTCT-exposed cardiac and skeletal muscle have not been experimentally evaluated.

    Cardiotoxic Cancer Treatment (CTCT) Promotes Oxidative Stress and Alters Monocyte/ macrophage Biology · 2019 · DOI

  • GPx4, Lipid Peroxidation, and Cell Death: Discoveries, Rediscoveries, and Open Issues.

    Reactive oxygen species (ROS) in cancer: from redox signaling and metabolic plasticity to therapeutic vulnerabilities · 2026 · DOI

  • Although the precise molecular signaling pathways were not investigated in the present study, the protective effects of tricin may be associated with suppression of oxidative stress mediated inflammatory pathways.

    Protective Effects of Tricin Against Oxldl-Stimulated Inflammatory and Oxidative Stress Responses in RAW 264.7 Cells · 2026 · DOI

  • ABSTRACT Cardiotoxicity induced by doxorubicin (Dox) significantly contributes to increased mortality among cancer patients, yet available pharmacological interventions remain scarce.

    Morroniside Attenuates Doxorubicin‐Induced Cardiotoxicity by Activating the PI3K/AKT/Nrf2/HO‐1 Pathway to Inhibit Ferroptosis and Oxidative Stress · 2026 · DOI

  • While both FAK and NRF2 are independently essential for gastrointestinal wound healing, their mechanistic relationship remains unclear.

    Role of Focal Adhesion Kinase and NRF2 Pathways in Gastrointestinal Wound Healing · 2026 · DOI

  • However, the specific effects and mechanisms by which RQMJ influences the transition from inflammation to cancer remain unclear.

    Renqing Mangjue modulates chronic atrophic gastritis inflammation-cancer transition via the cGMP–PKG/PI3K–AKT pathway · 2026 · DOI

  • Chronic oral exposure to TeA has been reported to induce dysplastic alterations in the esophageal mucosa of mice, while human biomonitoring data indicate an association between TeA exposure and esophageal cancer, although a causal relationship has not yet been established.

    Mechanistic characterization of tenuazonic acid-induced cellular stress responses in human esophageal KYSE-510 cells · 2026 · DOI

  • (rosemary) is widely consumed as a prominent source of natural antioxidants, its specific bioactive constituents and precise molecular targets against oxidative stress remain elusive.

    Rosmarinic acid, the key dietary antioxidant in <em>Rosmarinus officinalis</em> L. identified by integrated screening, targets PPAR&gamma; to activate Nrf2/NQO1 axis and mitigate oxidative stress · 2026 · DOI

  • Cannabidiol (CBD) has potent neuroprotective properties, but its exact molecular mechanism within the dopaminergic redox environment remains unclear.

    Cannabidiol confers neuroprotection against 6-OHDA toxicity by rescuing Nrf2 proteostasis and preserving mitochondrial integrity · 2026 · DOI

  • While the study shows that CYP71A12 becomes induced much stronger upon C. higginsianum challenge than abiotic stress in cyp71a13 mutants, the molecular mechanisms underlying this differential induction between biotic and abiotic stimuli remain unclear.

    Response of the Arabidopsis indolic secondary metabolite network to infection with Colletotrichum higginsianum · 2026 · DOI

  • The study assessed indolic secondary metabolism response to fungal infection in comparison to abiotic stresses, but some minor yet remarkable differences between biotic and abiotic stress responses were noted without full mechanistic explanation.

    Response of the Arabidopsis indolic secondary metabolite network to infection with Colletotrichum higginsianum · 2026 · DOI

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27 open questions have been extracted from the limitations and future-work passages of 165 Genomics, phytochemicals, and oxidative stress papers in our library. Each one below links back to the study that raised it, so you can read the original claim in context.

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