Search Results (203)

Alopecia is a multifactorial disorder in which immune, endocrine, metabolic, and microbial systems converge within the follicular microenvironment. In alopecia areata (AA), loss of immune privilege, together with interferon-γ- and interleukin-15-driven activation of the JAK/STAT cascade, promotes cytotoxic infiltration, whereas selective inhibitors, including baricitinib, ritlecitinib, and durvalumab, restore immune balance and permit anagen reentry. In androgenetic alopecia (AGA), excess dihydrotestosterone and androgen receptor signaling increase DKK1 and prostaglandin D2, suppress Wnt and β-catenin activity, and drive follicular miniaturization. Combination approaches utilizing low-dose oral minoxidil, platelet-rich plasma, exosome formulations, and low-level light therapy enhance vascularization, improve mitochondrial function, and reactivate metabolism, collectively supporting sustained regrowth. Elucidation of intracellular axes such as JAK/STAT, Wnt/BMP, AMPK/mTOR, and mitochondrial redox regulation provides a mechanistic basis for rational, multimodal intervention. Advances in stem cell organoids, biomaterial scaffolds, and exosome-based therapeutics extend treatment from suppression toward structural follicle reconstruction. Recognition of microbiome and mitochondria crosstalk underscores the need to maintain microbial homeostasis and redox stability for durable regeneration. This review synthesizes molecular and preclinical advances in AA and AGA, outlining intersecting signaling networks and regenerative interfaces that define a framework for precision and sustained follicular regeneration. Full article

The final trigger of oocyte maturation is a pivotal step in assisted reproductive technology (ART). Different molecules and protocols—including human chorionic gonadotropin (hCG), gonadotropin-releasing hormone agonists (GnRHa), the dual trigger, the double trigger, and emerging agents such as kisspeptin—have been investigated to optimize oocyte competence, embryo development, and pregnancy outcomes while minimizing the risk of ovarian hyperstimulation syndrome (OHSS). HCG remains the most widely used trigger, but its pharmacological profile is associated with a significant risk of OHSS. GnRHa has emerged as an alternative in antagonist cycles, abolishing the risk of severe OHSS but often requiring tailored luteal phase support. Several strategies, including hCG, GnRHa, and combined approaches, have shown improvements in specific outcomes such as the oocyte maturity (MII) rate, fertilization rate, embryo development parameters, and, in selected contexts, a reduction in OHSS risk. Kisspeptin represents a promising option; however, its use remains predominantly within the research setting, with clinical application still limited to early-phase or highly selected studies. Beyond the choice of molecule, the timing of trigger administration—adjusted to follicle size, estradiol concentrations, and progesterone levels—also influences oocyte competence and subsequent clinical outcomes. Triggering final oocyte maturation remains a multifaceted decision that should be individualized according to patient characteristics, ovarian response, and risk of OHSS. Although hCG remains the historical reference standard, accumulating but heterogeneous evidence suggests that GnRHa-based strategies, including dual-trigger protocols, may improve specific outcomes in selected patient subgroups. However, results across trials are inconsistent, particularly in poor responders, and any exposure to hCG maintains a residual risk of OHSS. Kisspeptin represents a promising but still experimental option, with current data largely limited to early-phase clinical studies in highly selected high-risk populations. Well-designed randomized trials are required to clarify the true impact of these strategies on live birth, to refine timing and dosing, and to better define which patients are most likely to benefit. Full article

Objectives: Fibroblast growth factor 9 (FGF9), a crucial member of the FGF family, functions as an intercellular signaling molecule involved in angiogenesis, embryogenesis, and tissue repair. Our previous study demonstrated that FGF9 expression in chicken hierarchical granulosa cells (Post-GCs) is regulated by LSD1 Ser54 phosphorylation and that FGF9 promotes cell proliferation. This study aims to analyze the expression and regulation of the FGF9 gene in chicken ovarian follicles and its genetic effect on laying traits in hens. Methods: Chicken FGF9 mRNA expression patterns were examined by real-time quantitative PCR (RT-qPCR). Detection of single nucleotide polymorphisms (SNPs) was performed using PCR amplification and Sanger sequencing. Transcription activity was compared using dual-luciferase reporter assay. Results: Following follicle selection, chicken FGF9 expression significantly decreased in granulosa cells (p < 0.05) while it increased in theca cells (p < 0.05). Hormonal treatments revealed differential regulation; estradiol and FSH downregulated FGF9 in both pre-hierarchical and hierarchical granulosa cells (p < 0.05), whereas progesterone exhibited opposing effects, suppressing expression in pre-hierarchical granulosa cells (Pre-GCs) but stimulating its expression in Post-GCs (p < 0.05). In theca cells, estradiol consistently inhibited FGF9 expression (p < 0.05), while FSH only affected FGF9 expression in pre-hierarchical follicles. Six SNPs in the promoter region (g.−1965G>A, g.−2177G>A, g.−2289G>A, g.−3669A>G, g.−3770A>G, g.−3906G>A) were identified, five of which (g.−1965G>A, g.−2177G>A, g.−2289G>A, g.−3669A>G, g.−3906G>A) showed significant associations with egg production traits. Notably, alleles A (g.−2289), G (g.−3669), and A (g.−3906) enhanced the transcription activity of chicken FGF9 in Pre-GCs. Conclusions: These findings provide novel insights into the expression pattern and regulatory mechanisms of chicken FGF9 during follicular development and identify some genetic markers for egg-laying traits in chickens. Full article

Follicle selection is a pivotal process that determines which dominant prehierarchical follicle will enter the preovulatory hierarchy in the hen ovary and directly affects egg-laying productivity, in which granulosa cells (GCs) are characterized by active proliferation and significantly enhanced FSHR mRNA expression. Increasing evidence has shown that the PI3K/Akt signaling pathway and its important target and effector FOXO1, which promotes GC apoptosis, play crucial roles in ovarian follicular development in mammals. To investigate the molecular mechanism by which follicle-stimulating hormone (FSH)-mediated forkhead box O1 (FOXO1) participates in follicle selection, we treated granulosa cells from 6–8 mm prehierarchical follicles of chickens with FSH and leptomycin B (LMB). The results showed that under FSH and/or LMB treatment, the expression levels of FSHR, FOXO1, and its phosphorylated forms (p-FOXO1) at the predicted protein kinase B (PKB/Akt) phosphorylation sites Thr²⁴, Ser²⁴⁸, and Ser³¹¹ were differentially regulated. The subcellular localization of p-FOXO1 in hen ovarian GCs was determined by Western blotting and immunofluorescence staining (IF) analysis. And the expression of FOXO1 was significantly reduced, whereas the expression of p-FOXO1 corresponding to the PKB phosphorylation sites Ser²⁴⁸ and Ser³¹¹ was noticeably boosted in cultured GCs induced by FSH, accompanied by exclusion of FOXO1 from the nucleus to the cytoplasm. Subsequently, the effects of the PI3K/Akt signaling pathway on phosphorylation levels and nuclear exclusion of p-FOXO1 at the sites Ser²⁴⁸ and Ser³¹¹ were examined. The results indicate that the PI3K/Akt-dependent phosphorylation at these sites directly resulted in nuclear exclusion of FOXO1 in ovarian GCs, in which the Ser²⁴⁸ site is more essential than the Ser³¹¹ site. Subsequently, the FSH-induced acetylation of FOXO1 mediated by the cAMP/PKA pathway can enhance the phosphorylation level of FOXO1 at the Ser²⁴⁸ site. In summary, our findings demonstrate that FSH induces FOXO1 phosphorylation, nuclear exclusion, and functional inactivation by activating the PI3K/Akt signaling pathway. Moreover, during follicular development and selection, FOXO1 acts as a pivotal mediator linking the PI3K/Akt and P62/Keap1/Nrf2 signaling pathways to regulate granulosa cell proliferation and apoptosis, thereby exerting a central regulatory role. Full article

Egg-laying performance in hens is regulated by complex molecular mechanisms within the hypothalamic–pituitary–gonadal (HPG) axis and ovarian follicles. This study employed integrative transcriptome profiling of primordial (PR), primary (PM), small white (SW), and small yellow (SY) follicles in hens with low and high egg-laying capacities to explain regulatory pathways influencing reproductive outcomes. Specific gene expression patterns were observed that correlated with follicular growth, steroidogenesis, and granulosa cell proliferation. Heatmap clustering and principal component analysis revealed transcriptional divergence between low- and high-laying hens, suggesting that coordinated changes in signaling pathways influence egg-laying performance. High-laying hens intricated an upregulation of the PI3K-AKT-FOXO3, TGF-β, and Wnt/β-catenin pathways, which facilitate early follicular development, granulosa cell proliferation, and folliculogenesis. Higher phosphorylation of AKT and reduced nuclear FOXO3 activity were associated with enhanced primordial follicle growth. Increased TGF-β signaling, as demonstrated by higher levels of SMAD2/3/4 and cell cycle regulators, promoted granulosa cell proliferation in primary follicles (PMF). In SWF, higher levels of β-catenin and its downstream genes, such as c-Myc and cyclin D1, promoted follicle development. High-laying hens revealed increased expression of FSHR, CYP19A1, 17β-HSD, CYP1A1, and CYP1B1 in SYF, signifying enhanced FSH level and steroidogenesis. Similarly, low-laying hens exhibited downregulation of key genes, suggesting reduced follicular development and hormone signaling. These findings identify key regulatory networks and molecular markers associated with reproductive performance, providing targets for genetic selection and interventions to enhance egg production while reducing the risk of hormonal overstimulation. Full article

This study investigates the regulatory role of circFBN1 in chicken follicular granulosa cells (GCs) and its underlying molecular mechanisms through the miR-206/E2F5 pathway. circFBN1 was found to significantly enhance GC proliferation and inhibit apoptosis, as evidenced by increased expression of proliferation-related genes (PCNA, CDK1, and CCND1) and decreased expression of apoptosis-related genes (Caspase-3). Additionally, circFBN1 overexpression promoted the secretion of estradiol (E2) and progesterone (P4) by upregulating steroidogenesis-related genes (StAR and CYP11A1). Mechanistic studies revealed that circFBN1 functions as a molecular sponge for miR-206, thereby alleviating its inhibitory effect on the target gene E2F5. Dual-luciferase reporter assays confirmed the specific binding between circFBN1 and miR-206. Overexpression of miR-206 had the opposite effects, inhibiting GC proliferation, inducing apoptosis, and reducing E2 and P4 secretion by downregulating StAR and CYP11A1. Furthermore, E2F5 was identified as a direct target of miR-206, and its knockdown significantly reduced GC proliferation, increased apoptosis, and decreased steroid hormone secretion. These findings elucidate the regulatory mechanisms of the circFBN1/miR-206/E2F5 axis in avian follicle development and provide potential molecular targets for improving poultry reproductive performance. Future research should focus on exploring the upstream regulators of this axis and its interactions with other signaling pathways. Full article

Background: G-protein-coupled receptors (GPCRs) play pivotal roles in tumor growth and progression. Among these, the luteinizing hormone-releasing hormone receptor (LHRH-R) and follicle-stimulating hormone receptor (FSH-R) represent promising translational targets, unlike luteinizing hormone receptors (LH-Rs). Indeed, both LHRH-R and FSH-R are selectively expressed in various cancers and their vasculature, offering opportunities for receptor-mediated imaging and therapy. Objectives: This systematic review aims to evaluate radiolabeled LHRH- and FSH-derivative biomolecules, including peptides, monoclonal antibodies and nanocarriers, for their applications in cancer diagnosis and treatment. Methods: The systematic review was conducted following PRISMA 2020 guidelines. A systematic search of PubMed, Scopus and Web of Science was conducted for studies published between 2005 and 2025. A total of 248 records were identified, and 156 articles were screened after removing duplicate records. Two authors independently selected eligible studies. Quality of evidence was assessed by the Quality Assessment of Diagnostic Accuracy Studies (QUADAS) approach. Results: A total of 25 studies met the inclusion criteria and were included in the final review. Radiolabeled LHRH and FSH derivatives showed receptor-specific tumor localization in both preclinical and clinical applications. FSH-R expression in tumor blood vessels supports its potential as a biomarker for early cancer diagnosis. FSHβ-derived peptides exhibit improved pharmacokinetics compared to monoclonal antibodies in PET imaging. LHRH analogues, particularly D-Lys⁶-modified peptides, proved effective for SPECT, PET and therapeutic applications, particularly in breast and prostate cancer. The integration of radiolabeled LHRH and FSH derivatives with nanocarriers further enhanced probe stability and tumor targeting, increasing tumor accumulation and image contrast compared to free peptide. Conclusions: Radiopharmaceuticals targeting LHRH-R and FSH-R are promising tools for cancer imaging and treatment. Advances in nanotechnology enhance delivery precision and reduce systemic toxicity, thereby increasing its translational promise in oncology. Full article

Background: Selective serotonin reuptake inhibitors (SSRIs) are widely prescribed, yet their direct impact on ovarian function remains poorly understood. While serotonin signaling is known to occur within the ovarian follicle, the specific molecular consequences of its disruption by SSRIs are unclear. This study aimed to elucidate the direct, intra-ovarian mechanisms by which fluoxetine, a common SSRI, affects follicular development and oocyte competence. Methods: We administered fluoxetine (20 mg/kg) or vehicle daily for seven days to both prepubertal and adult female mice to model short-term therapeutic exposure. Results: Fluoxetine treatment successfully blocked peripheral serotonin uptake, reducing serum levels by over 90%. Crucially, this occurred without altering circulating levels of estradiol, FSH, or LH and without disrupting the estrous cycle, indicating a mechanism independent of the central hypothalamic–pituitary–gonadal axis. Instead, we pinpoint a direct ovarian effect: fluoxetine inhibited serotonin transport activity in oocytes and significantly downregulated the expression of the pivotal oocyte-derived growth factor Gdf9. This was accompanied by reduced expression of genes crucial for granulosa cell function (Lhr, Fshr) and steroidogenesis (Cyp19a1). Functionally, these molecular changes manifested as a decline in oocyte quality and a significant reduction in ovulation rates in adult mice. Notably, these detrimental effects were more pronounced in prepubertal mice, indicating a heightened vulnerability during early follicular development. Conclusions: Our findings reveal a direct, intra-ovarian mechanism of fluoxetine-induced disruption. By inhibiting oocyte serotonin transport and downregulating GDF9, fluoxetine impairs critical oocyte–granulosa cell communication, thereby compromising oocyte competence and reducing fertility outcomes. This work identifies follicular development as a critical window of susceptibility to SSRI exposure, holding significant clinical implications for reproductive-aged and adolescent populations. Full article

Background: Hidradenitis suppurativa (HS) is a chronic, recurrent skin disease that significantly impairs patients’ quality of life both physically and mentally. It often requires a complex treatment process. Laser therapy, which is highly effective and well-tolerated, is an effective alternative to pharmacological treatment. This review aimed to synthesize information on laser therapy for HS, highlighting its clinical outcomes. In the current management guidelines for hidradenitis suppurativa, laser therapy is listed as one of the recommended procedural treatment options, applicable at different stages of disease severity (Hurley I–III). Methodology: This systematic review was conducted using the PubMed and Embase databases, regardless of publication year, in accordance with the PRISMA guidelines. Applied key search terms were: “laser AND (hidradenitis suppurativa OR acne inversa)”. A total of 26 relevant studies were identified, and their data were extracted. Results: The CO₂ laser is mainly used in advanced stages of the disease (Hurley II–III). It allows effective removal of lesions with a minimal risk of relapse and a good aesthetic effect. The Nd:YAG (neodymium-doped yttrium aluminum garnet; Nd: Y₃Al₅O₁₂) laser is effective at various stages of the disease (Hurley I–III) by reducing inflammation and destroying hair follicles, thereby reducing disease symptoms. IPL (intense-pulse light) therapy, or the combination of IPL with radiofrequency (RF), known as LAight^®, delivers significant clinical improvement and enhanced quality of life, especially in less advanced cases. The diode laser works precisely and deeply, leading to the selective destruction of hair follicles and fistulas. The Alexandrite laser (755 nm) also limits hair follicle occlusion and is particularly effective in patients with lighter skin phototypes. Conclusions: In modern dermatology, laser therapy is a reliable treatment for HS, contributing to effective regression of the disease at all stages. Combination strategies seem to improve clinical outcomes and enable a more personalized approach to HS, which is essential as various factors influence therapeutic efficacy. Further, larger-scale studies are needed to validate long-term outcomes and establish clinical guidelines. Full article

Reproductive outcomes following synchronized ovulation protocol in beef cattle are influenced by multiple factors, making protocol selection based on farm-specific conditions essential. This retrospective study analyzed the relationship between pregnancy rates and associated factors under the CIDR (GnRH with CIDR insertion–PGF_2α with CIDR removal–GnRH), GPG (GnRH–PGF_2α–GnRH), and GPPG (GnRH–PGF_2α–PGF_2α–GnRH) protocols in Hanwoo cattle. The highest pregnancy rate was observed with the CIDR protocol (58.3%), whereas the GPG protocol yielded the lowest (47.5%). The CIDR protocol demonstrated superior suitability compared with the GPG protocol in first service (61.0% vs. 47.0%) and young breeding cattle (parity: 0–2; 61.6–70.0% vs. 47.5–48.6%). The dominant follicle size strongly associated with pregnancy success was 13–16 mm, and the CIDR protocol induced these follicles more frequently than the GPG protocol (50.2% vs. 35.5%). Although interpretive bias may exist from data collected from pregnant animals only, CIDR protocol significantly increased luteinizing hormone levels compared to GPG. The GPPG protocol produced outcomes that were improved relative to the GPG protocol and statistically comparable to the CIDR protocol. These findings addressed the study’s objective, identifying optimal synchronized ovulation strategies and underscoring reproductive management importance for Korean Hanwoo operations. Full article

Recent enthusiasm has surrounded the homeostatic roles that polyamines have in a variety of cell types. Thus, the purpose of this exploratory in vitro study was to determine how spermidine (SPD), a polyamine commonly consumed as a nutritional supplement, affected general markers of cellular health and function in human primary epidermal keratinocytes. Commercial HEKa cells were seeded onto either six-well (transcriptomics and immunoblotting) or 96-well culture plates (viability, ATP, and JC-1 assays) and cultured to ~90+% confluency through complete growth media (CGM) changes every 48 h. Once cells reached this level of growth, treatments included either CGM + phosphate-buffered saline (PBS control, or CTL), CGM + 1 µM SPD, and CGM + 10 µM SPD for either 6 or 24 h depending upon the outcome being assessed. Cellular ATP levels were not significantly affected by 1 µM or 10 µM SPD treatments lasting 24 h. However, cell counts were 9% greater (p = 0.007) when comparing 24 h 10 µM versus CTL treatments indicating increased cell viability. Transcriptomic analyses indicated that 6 h treatments with 10 µM SPD significantly altered 162 transcripts versus non-treated CTL cells (65 up-regulated and 97 down-regulated, p < 0.01). Four pathways were predicted to be enriched based on differential gene expression including protein deubiquitination (GO:0016579), membrane lipid biosynthesis (GO:0046467), DNA metabolic process (GO:0006259), and cell cycle process (GO:0022402). Additionally, the HR gene (essential for keratinocyte hair follicle formation) was significantly up-regulated at the mRNA level with 6 h 10 µM SPD, and immunoblotting confirmed a 96% increase in protein levels with 24 h 10 µM SPD treatments, albeit this did not reach statistical significance (p = 0.102). Pan-keratin protein content was also 60% greater in the 1 µM and 10 µM 24 h treatments than CTL (p ≤ 0.029). Finally, although select markers of mitochondrial content and biogenesis were not significantly altered with 6 h and 24 h treatments, mitochondrial membrane potential (an aspect of mitochondrial function) was 84% greater with 24 h 1 µM versus CTL (p < 0.001). In conclusion, these preliminary screening experiments in unperturbed human keratinocytes suggest that exogenous SPD positively affects various aspects of homeostasis by stimulating transcriptomic and functional alterations (e.g., increased cell viability and enhanced keratinocyte protein levels). Full article

Fertility potential ever more diminishes due to the complex, multifactorial, and still not entirely clarified process of reproductive aging in women and men. Gamete quality and reproductive lifespan are compromised by biologic factors like mitochondrial dysfunction, increased oxidative stress (OS), and incremental telomere shortening. Clinically confirmed biomarkers, including follicle-stimulating hormone (FSH) and anti-Müllerian hormone (AMH), are used to estimate ovarian reserve and reproductive status, but these markers have limited predictive validity and an incomplete representation of the complexity of reproductive age. Recent advances in artificial intelligence (AI) have the capacity to address the integration and interpretation of disparate and complex sets of data, like imaging, molecular, and clinical, for consideration. AI methodologies that improve the accuracy of reproductive outcome predictions and permit the construction of personalized treatment programs are machine learning (ML) and deep learning. To promote fertility evaluations, here, as part of its critical discussion, the roles of mitochondria, OS, and telomere biology as latter-day biomarkers of reproductive aging are presented. We also address the current status of AI applications in reproductive medicine, promises for the future, and applications involving embryo selection, multi-omics set integration, and estimation of reproductive age. Finally, to ensure that AI technology is used ethically and responsibly for reproductive care, model explainability, heterogeneity of data, and other ethical issues remain as residual concerns. Full article

Tooth development (odontogenesis) is regulated by interactions between epithelial and mesenchymal tissues through signaling pathways such as Bone Morphogenetic Protein (BMP), Wingless-related integration site (Wnt), Sonic Hedgehog (SHH), and Fibroblast Growth Factor (FGF). Mesenchymal stem cells (MSCs) derived from dental tissues—including dental pulp stem cells (DPSCs), periodontal ligament stem cells (PDLSCs), and dental follicle progenitor cells (DFPCs)—show promise for regenerative dentistry due to their multilineage differentiation potential. Epigenetic regulation, particularly DNA methylation, is hypothesized to underpin their distinct regenerative capacities. This study reanalyzed publicly available DNA methylation data generated with Illumina Infinium HumanMethylation450 BeadChip arrays (450K arrays) from DPSCs, PDLSCs, and DFPCs. High-confidence CpG sites were selected based on detection p-values, probe variance, and genomic annotation. Principal Component Analysis (PCA) and hierarchical clustering identified distinct methylation profiles. Functional enrichment analyses highlighted biological processes and pathways associated with specific methylation clusters. Noncoding RNA analysis was integrated to construct regulatory networks linking DNA methylation patterns with key developmental genes. Distinct epigenetic signatures were identified for DPSCs, PDLSCs, and DFPCs, characterized by differential methylation across specific genomic contexts. Functional enrichment revealed pathways involved in odontogenesis, osteogenesis, and neurodevelopment. Network analysis identified central regulatory nodes—including genes, such as PAX6, FOXC2, NR2F2, SALL1, BMP7, and JAG1—highlighting their roles in tooth development. Several noncoding RNAs were also identified, sharing promoter methylation patterns with developmental genes and being implicated in regulatory networks associated with stem cell differentiation and tissue-specific function. Altogether, DNA methylation profiling revealed that distinct epigenetic landscapes underlie the developmental identity and differentiation potential of dental-derived mesenchymal stem cells. This integrative analysis highlights the relevance of noncoding RNAs and regulatory networks, suggesting novel biomarkers and potential therapeutic targets in regenerative dentistry and orthodontics. Full article

The transforming growth factor-beta (TGF-β) superfamily plays a crucial role in regulating female reproductive traits, particularly litter size, in small ruminants, such as sheep and goats. This review comprehensively examines the molecular mechanisms through which TGF-β superfamily members—including bone morphogenetic proteins (BMPs), growth differentiation factor 9 (GDF9), inhibin (INHA and INHB), and associated signaling genes—influence ovarian follicular development, ovulation rate, and ultimately, litter size. We synthesize recent findings on polymorphisms in key genes, such as BMPR1B, BMP15, GDF9, inhibins and SMADs family genes, across diverse sheep and goat breeds worldwide. The manuscript highlights how specific mutations in these genes create an intricate signaling network that modulates granulosa cell proliferation, follicular sensitivity to FSH, and the prevention of dominant follicle selection. These molecular interactions result in increased ovulation rates and larger litter sizes in prolific breeds. The gene dosage effects observed in heterozygous versus homozygous mutation carriers further illuminate the complex nature of these reproductive regulations. This improved the understanding of the genetic basis for prolificacy provides valuable insights for marker-assisted selection strategies aimed at enhancing reproductive efficiency in small ruminant breeding programs, with significant implications for improving livestock productivity and economic outcomes. Full article

Background: Intraovarian platelet-rich plasma (PRP) has emerged as a novel intervention at the intersection of reproductive medicine and regenerative biology. As women with diminished ovarian reserve (DOR), poor response to stimulation, or premature ovarian insufficiency (POI) seek fertility solutions, PRP provides a scientifically plausible—yet exploratory—strategy to restore or augment ovarian function. The proposed pathways include the stimulation of local stem cells, tissue remodeling, neoangiogenesis, and the potential reawakening of dormant follicles. Methods: This narrative review critically synthesizes the existing literature on intraovarian PRP therapy. It draws from published case series, pilot studies, and preclinical data to evaluate the biological rationale, clinical outcomes, and current limitations of PRP use in women with DOR and POI. Results: Early clinical findings, albeit limited to modest case series and pilot investigations, reveal promising outcomes such as improved ovarian reserve markers, menstrual restoration, and infrequent spontaneous pregnancies in women who had previously been unresponsive to treatment. However, the variability in preparation techniques, patient selection criteria, and outcome measures limits the generalizability of these results. Conclusions: While intraovarian PRP presents an exciting frontier in reproductive medicine, the absence of defined protocols, controlled trials, and long-term safety data underscores its experimental nature. Future research should focus on standardizing methodologies, conducting randomized controlled trials, and elucidating the molecular mechanisms underlying observed clinical effects to establish PRP’s role in managing poor ovarian response and POI. Full article