Genistein, as a potential adjunctive therapeutic candidate for PCOS, has shown promise

The gap

Evidence profile

Sourced from the future work of the source papers, classified as general, spanning 3 journals.

Supporting evidence — 3 representative gaps

• Advances in Polydopamine-Based Nanoplatforms: Antioxidant Mechanisms and Applications in Oxidative Stress-Mediated Diseases (2026) · Nano-Micro Letters · doi

  With the rapid development of nanobiomaterials, PDA- based nanoplatforms have demonstrated immense transla- tional potential in intervening in oxidative stress-mediated diseases. This review systematically summarizes the unique physicochemical properties of PDA alongside its antioxidant mechanisms such as ROS-scavenging and enzyme-mimick- ing activities, and its structural engineering strategies and diverse morphologies in constructing delivery systems. Building upon this foundation, we highlight the multidi- mensional framework of PDA in the intervention of oxida- tive stress diseases. Specifically, we systematically summa- rize its core strategic roles in breaking the self-amplifying ROS-inflammation loop, overcoming complex biological barriers, remodeling the regenerative microenvironment, regulating programmed cell death cascades, and achieving multimodal synergistic therapy. These synergistic strategies significantly broaden the boundaries of antioxidant interven- tions. By systematically analyzing the inherent biocompat- ibility and stimuli-responsive behavior of PDA alongside its dual function as both a structural carrier and an active redox regulator, this article evaluates its practical feasibility and therapeutic efficacy as a nano-antioxidant to provide a solid theoretical basis and design paradigm for the future develop- ment of next-generation PDA-based nanoplatforms featuring high targeting capability and deep synergistic therapeutic functions. However, despite these advancements, the transi- tion from fundamental research to clinical application still requires resolving several conceptual and methodological limitations. Future research should prioritize the following four dimensions to enhance the therapeutic precision and translational potential of PDA-based nano-antioxidants. 1. Enhancing catalytic efficiency through single-atom engineering. The inherent kinetics of ROS scavenging by PDA are often insufficient to address the character- istic acute oxidative bursts in diseases such as sepsis or ischemia–reperfusion injury, where integrating sin- gle-atom catalysis (SAC) represents a frontier direc- tion for overcoming this kinetic bottleneck [251]. By utilizing the robust metal-chelating capability of PDA to anchor transition metal single atoms such as Fe, Cu, or Mn within its polymer backbone researchers can pro- mote strong metal-support interactions. Indeed, recent pioneering studies have demonstrated that anchoring isolated transition metal atoms onto a melanin-like net- work can achieve orders-of-magnitude amplification in nanozyme or antioxidant activities [84]. This strategy not only maximizes atomic utilization but also signifi- cantly reduces the activation energy for ROS degrada- tion to transform PDA from a stoichiometric scavenger into a highly efficient catalytic platform for selective ROS clearance. 2. Addressing the ROS paradox through stimuli-responsive systems.

  generalfuture work
  Keywords: antioxidant metal based diseases systematically synergistic therapeutic tion nanoplatforms potential oxidative stress alongside scavenging activities
• Genistein in polycystic ovary syndrome: mechanisms, preclinical evidence, and translational potential (2026) · Frontiers in Global Women's Health · doi

  Genistein, as a potential adjunctive therapeutic candidate for PCOS, has shown promise in improving metabolic homeostasis, regulating sex hormones, and restoring ovarian function. To overcome its limitations, researchers have been developing novel delivery systems to enhance genistein’s solubility, stability, and targeting efficiency. A variety of drug delivery platforms have been designed to protect and stabilize genistein and address the challenge of its low bioavailability (102). Previous studies have shown that drug-loaded nanoparticles, solid lipid nanoparticles (SLNs), and nanostructured lipid carriers have been explored as potential therapeutic approaches for multiple diseases (103, 104). These systems can significantly improve genistein’s solubility, stability, and absorption, thereby increasing oral bioavailability and potentially enhancing therapeutic responses by improving tissue permeability (18, 20). In addition, genistein formulations may be further optimized to improve routes of administration, including tablet, microparticle, and micellar systems (105). With these advances, low bioavailability may no longer represent a major barrier to clinical translation. Given that genistein is a relatively mild phytoestrogen and that monotherapy may offer limited efficacy in patients with severe PCOS, future research should focus on evaluating its potential as an adjunctive treatment for PCOS and investigating its effects across different PCOS phenotypes. Studies should also examine the synergistic effects of genistein with conventional therapies, identify the optimal therapeutic dose, and minimize adverse effects. Combination therapy has shown encouraging synergistic potential. For example, co-administration with metformin may further improve insulin sensitivity and reduce gastrointestinal (106). When adverse effects associated with metformin combined with traditional ovulation-inducing agents, genistein may help optimize the ovarian microenvironment and improve follicular quality and ovulation success. Likewise, in combination with dietary supplements such as quercetin, it may exert Frontiers in Global Women’s Health 09 frontiersin.org Wang et al. 10.3389/fgwh.2026.1836617 complementary effects on modulation (107). lipid reduction and immune

  generalfuture work
  Keywords: genistein effects potential therapeutic pcos improve systems bioavailability lipid adjunctive improving ovarian delivery solubility stability
• Oxidative stress and inflammation in breast cancer: Mechanistic interactions and clinical implications (2026) · World Journal of Clinical Cases · doi

  The pathogenesis and progression of BC are closely linked to the interaction between oxidative stress and inflammation and remain a major cause of morbidity and mortality in women worldwide. Because BC is very heterogeneous, including hormone receptor- positive, HER2-positive, and TNBC, it is important to understand the underlying molecular mechanisms that drive its onset, progression, and resistance to treatment[45]. New therapeutic strategies use nanotechnology to deliver substances that modulate ROS levels in tumors. Lipid nanoparticles offer increased drug-loading capacity, stability, reduced toxicity, and improved targeting compared to traditional formulations[46]. In preclinical models, nanomaterials designed to produce cytotoxic ROS only in tumor cells are effective in disrupting the redox balance and causing DNA damage or lipolysis[47]. These platforms can also be designed for combination therapies-e.g., chemotherapy- in which the release of doxorubicin-loaded platelets has been shown to induce immunogenic cell death in TNBC models by releasing DAMPs, which activate dendritic cells and promote antitumor immunity in combination with immune checkpoint blockade[48]. The complex interaction between oxidative stress and ER stress complicates BC pathophysiology. Accumulation of misfolded proteins in the ER lumen causes ER stress 16 / 34 and triggers the unfolded protein response (UPR), which is designed to restore proteostasis. Through overlapping signaling pathways, ER stress and ROS production are closely related in multiple myeloma, a hematological malignancy similar to solid tumors. Through activation of the ER by ROS production in a self-sustaining cycle, prolonged ER stress can lead to apoptosis[49]. In highly metastatic BC such as TNBC, protein disulfide isomerase (PDI), an abundant ER enzyme involved in protein folding, was identified as a potential therapeutic target. PDI inhibition interferes with UPR signaling and induces apoptosis by sustained stress[50]. Physical activity and other lifestyle factors also influence BC risk and progression by altering the regulation of oxidative stress and inflammation. Exercise improves mitochondrial biogenesis in skeletal muscle, enhances antioxidant protection, reduces oxidative damage associated with aging, and reduces endothelial dysfunction. All these factors contribute to a healthier aging profile and may indirectly affect BC outcomes by altering the systemic redox state[51]. While fasting may not be feasible for cancer patients, it can be a beneficial tool in cancer prevention and treatment. Intermittent fasting exerts its effects by regulating circulating insulin and IGF-1 levels, metabolic and oxidative-inflammatory pathways, strengthening the autophagic process, and sup

  generalfuture work
  Keywords: stress oxidative progression tnbc designed protein closely interaction inflammation positive treatment therapeutic levels tumors models

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