Estrogen metabolites increase nociceptor hyperactivity in a mouse model of uterine pain

Xie, Zili; Feng, Jing; Cai, Tao; McCarthy, Ronald; Eschbach, Mark D.; Wang, Yuhui; Zhao, Yue; Yi, Zhihua; Zang, Kaikai; Yuan, Yi; Hu, Xueming; Li, Fengxian; Liu, Qin; Das, Aditi; England, Sarah K.; Hu, Hongzhen

doi:10.1172/jci.insight.149107

Cited by 10 publications

(2 citation statements)

References 67 publications

(73 reference statements)

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“…Several pathophysiological pathways point to biological plausibility between tear gas and menstrual disruptions, including it metabolizing into cyanide and subsequent hypoxia and adrenal and thyroid dysregulation, indicating potential endocrine disruption ( 24 ). Additionally, CS gas is known to activate pain receptors ( 25 ) that are also involved in pain related to dysmenorrhea ( 26 , 27 ), endometriosis ( 27 , 28 ), and other uterine conditions ( 29 ), helping to explain uterine cramping reported by participants.…”

Section: Discussionmentioning

confidence: 99%

More than tears: associations between exposure to chemical agents used by law enforcement and adverse reproductive health outcomes

Hassan,

Ojanen-Goldsmith,

Hing

et al. 2023

Front. Epidemiol.

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Despite routine law enforcement use of chemical agents for crowd control, the reproductive health safety profiles of these products are unknown. Moreover, limited evidence has documented a link between such exposures and adverse reproductive health outcomes including abnormal uterine bleeding and potential pregnancy disruption. This cross-sectional study examined reproductive outcomes in adults with uteri exposed to chemical agents used by law enforcement, more commonly known as “tear gas”. Participants were recruited through social media in the wake of police violence protests. Of the 1,276 participants included in analysis, 83% reported experiencing at least one of the outcomes of interest, included uterine cramping (69%), early menstrual bleeding (55%), breast tenderness (30%), and delayed menstrual bleeding (19%). Chemical agent exposure was significantly associated with higher odds of an adverse reproductive health outcome, those with 5 days or more of exposure have 2.6 times the odds (CI: 1.61, 4.22) of adverse outcomes and having a perception that one's menstruation may fluctuate according to psychosocial stressors was associated (OR = 1.94, CI: 1.36, 2.79) with a higher odds of an adverse reproductive health experience. These findings suggest a potential relationship between exposure to chemical agents and adverse reproductive health outcomes. Given the pervasive use of these chemical agents and their potential for reproductive health harm, further investigation into the safety of these products and their impacts on individual and community health is warranted urgently.

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Section: Discussionmentioning

confidence: 99%

More than tears: associations between exposure to chemical agents used by law enforcement and adverse reproductive health outcomes

Hassan,

Ojanen-Goldsmith,

Hing

et al. 2023

Front. Epidemiol.

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“… 428 , 429 Other estrogen metabolites, including 2- and 4-HEMs and 2- or 4-OHE1, directly simulate TRPV1 and TRPA1, contributing to the dramatical reduction in uterine pain threshold. 430 Conversely, testosterone has been proved to have protective effects against nociceptive pain. 431 …”

Section: Mechanisms Of Pain Sexual Dimorphismmentioning

confidence: 99%

Pathology of pain and its implications for therapeutic interventions

Cao,

Xu,

Shi

et al. 2024

Sig Transduct Target Ther

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Pain is estimated to affect more than 20% of the global population, imposing incalculable health and economic burdens. Effective pain management is crucial for individuals suffering from pain. However, the current methods for pain assessment and treatment fall short of clinical needs. Benefiting from advances in neuroscience and biotechnology, the neuronal circuits and molecular mechanisms critically involved in pain modulation have been elucidated. These research achievements have incited progress in identifying new diagnostic and therapeutic targets. In this review, we first introduce fundamental knowledge about pain, setting the stage for the subsequent contents. The review next delves into the molecular mechanisms underlying pain disorders, including gene mutation, epigenetic modification, posttranslational modification, inflammasome, signaling pathways and microbiota. To better present a comprehensive view of pain research, two prominent issues, sexual dimorphism and pain comorbidities, are discussed in detail based on current findings. The status quo of pain evaluation and manipulation is summarized. A series of improved and innovative pain management strategies, such as gene therapy, monoclonal antibody, brain-computer interface and microbial intervention, are making strides towards clinical application. We highlight existing limitations and future directions for enhancing the quality of preclinical and clinical research. Efforts to decipher the complexities of pain pathology will be instrumental in translating scientific discoveries into clinical practice, thereby improving pain management from bench to bedside.

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