Uterine leiomyomas or fibroids are a common but pernicious benign tumor impacting between 70–80% of women of reproductive age. Despite their high prevalence, the etiology of uterine fibroids is not fully understood. This review aims to highlight the distinct metabolic features that uterine fibroids adopt to meet biosynthetic demands, support proliferation, extracellular matrix production, survival, and fibrosis. Specifically, we posit the role of glycolytic reprogramming—an adaptation in fibrosis across organs (lung, kidney, heart, and liver) as a major contributor to uterine fibroid development. Previous genetic, transcriptomic, proteomic, and metabolic studies have drawn strong links between metabolism and uterine fibroid biology and identified genotype-specific metabolic alterations such as fumarate hydratase (FH) deficiency and mediator of RNA polymerase II transcription (MED12) gene mutations. Studies in non-uterine models have linked glycolysis to ECM production and fibrosis through activation of transforming growth factor-beta (TGF-β) and the canonical Wnt pathway (Wnt/β-catenin) signaling, supporting them as potential key pathways in uterine fibroid pathogenesis via glycolytic reprogramming. Other metabolic regulators, such as hypoxia-inducible factor 1-alpha (HIF-1α), mammalian target of rapamycin (mTOR), and phosphoinositide 3-kinase/protein kinase B (PI3K/Akt), may also sustain the fibrotic phenotype through coupling signaling that drives ECM production to metabolic programming. Overall, the proposed metabolic perspective of uterine fibroid pathogenesis invites further exploration of mechanistic investigation in uterine-specific models and therapeutic targeting through larger cohort studies.

Uterine fibroids (leiomyomas) are common benign smooth muscle tumors that impose substantial symptom burden and healthcare costs worldwide. Although uterine fibroid (leiomyoma) pathogenesis is multifactorial, hypoxia has emerged as a key feature of the uterine fibroid (leiomyoma) microenvironment, particularly within poorly perfused tumor cores. Hypoxia-inducible factor-1α (HIF-1α) is a central transcriptional regulator of cellular adaptation to low oxygen and coordinates downstream programs that support angiogenesis, metabolic reprogramming, cell survival, and extracellular matrix (ECM) remodeling. In uterine fibroids (leiomyomas), these HIF-1α–dependent processes intersect with steroid hormone signaling, growth factor pathways, inflammatory mediators, and redox imbalance, together promoting tumor persistence and progressive fibrosis. This review synthesizes the molecular regulation of HIF-1α, highlights major HIF-linked effector pathways relevant to uterine fibroid (leiomyoma) biology, and emphasizes mechanistic crosstalk with estrogen- and progesterone-responsive signaling, TGF-β/SMAD-driven fibrosis, NF-κB-mediated inflammation, and metabolic checkpoint pathways including mTOR and AMPK. Finally, we evaluate emerging therapeutic strategies that target HIF-1α directly or indirectly through upstream regulators.

Incarcerated postpartum individuals with opioid use disorder (OUD) are vulnerable to poor health outcomes, but care provision in custody for this population is variable. Addressing their distinct needs is crucial for improving correctional health care for postpartum people. In this paper wea document challenges jail staff experience providing postpartum care, and describe shifts in jail staff knowledge and practice changes related to postpartum care that may be attributable to participation in a training resource for perinatal OUD in corrections. We developed a web-based resource for jail staff called “Maternal Opioid Use Disorder Management and Care Resources in Custody” (MOMCARE). From May 2024 to January 2026, we conducted a 12-month pilot MOMCARE intervention at five jails of varying sizes across the United States. We collected facility data on postpartum services, provided ongoing facilitation activities, and conducted qualitative interviews with jail staff to explore postpartum care challenges and opportunities. Through a needs assessment survey and qualitative interviews with staff at baseline, we documented gaps and challenges in service provision for postpartum people. Through ongoing interviews and facilitation activities, jail staff reported promising practice changes including systematically screening for postpartum status at intake, streamlining lactation support processes, and assessing postpartum mental health using validated screening tools. Jail staff also learned that it is safe and recommended for postpartum people to breastfeed while on medications for OUD. Jail staff were receptive to educational and support tools. MOMCARE prompted jails to make changes that align with best practices for postpartum care.