Tranylcypromine, a lysine-specific demethylase 1 (LSD1) inhibitor, suppresses lesion growth and improves generalized hyperalgesia in mouse with induced endometriosis

Qunyan Sun, Sun Qunyan, Ding Ding, Xishi Liu, Sun-Wei Guo, Sun‐Wei Guo
Reproductive biology and endocrinology : RB&E · 2016 · vol. 14(1) , pp. 17 · doi:10.1186/s12958-016-0154-0 · PMID:27062244 · PMC4826530 · W2319034373
article OA: gold CC0 ⤵ 16 in-corpus citations
📄 Open PDF View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

Tranylcypromine, an LSD1 inhibitor, suppressed lesion growth and improved hyperalgesia in mice with induced endometriosis by reducing proliferation, angiogenesis, and H3K4 methylation, thereby arresting EMT.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 ⓘ

This paper studied whether tranylcypromine (TC), an LSD1 (lysine-specific demethylase 1) inhibitor, can suppress ectopic lesion growth and improve generalized hyperalgesia in a mouse model of induced endometriosis. Forty-seven female C57BL/6 mice underwent endometriosis-inducing or sham surgery, then received untreated, low-dose TC, or high-dose TC (with a specificity control that also received high-dose TC) and underwent hotplate testing before induction, before treatment, and before sacrifice, followed by lesion size measurement and immunohistochemistry for proliferation, angiogenesis, H3K4 methylation, and EMT markers. TC treatment significantly and dose-dependently reduced lesion size and improved generalized hyperalgesia while lowering immunoreactivity to proliferation/angiogenesis markers and H3K4 methylation, coinciding with arrested EMT and lesion growth. A major caveat explicitly stated is that trial registration was not applicable, and the study lacks a detailed report of long-term outcomes or behavioral specificity beyond the hotplate/generalized hyperalgesia readouts. This paper is centrally about endometriosis — it tests LSD1 inhibition by tranylcypromine as an epigenetic therapeutic strategy to reduce lesion growth and generalized hyperalgesia in an induced mouse model.

Read from the paper's body, not the abstract. Not a substitute for reading the paper. No clinical advice. How this works

Abstract

BACKGROUND: Growing evidence indicates that endometriosis is an epigenetic disease. Encouragingly, histone deacetylases (HDACs) and DNA methyltransferases have been shown to be promising targets by numerous in vitro studies. However, only a few studies have shown promising effects of HDAC inhibition in preclinical studies in endometriosis. While lysine-specific demethylase 1 (LSD1) is recently found to be aberrantly expressed in endometriosis, and that the treatment of endometriotic stromal cells with tranylcypromine (TC), an LSD1 inhibitor, significantly reduced cellular proliferation, cell cycle progression, and invasiveness, the in vivo effect of TC treatment is currently lacking. This study sought to evaluate the effect of TC in a mouse model of endometriosis. METHODS: Forty-seven female C57BL/6 mice were used in this experimentation. All mice, except those randomly selected to form Sham surgery (M) and specificity control (S) groups, received an endometriosis-inducing surgery. Group S was set up mainly to ensure that the reduced generalized hyperalgesia in mice treated with TC is not due to any possible analgesic effect of TC, but rather resulting from the treatment effect specific to endometriosis. Two weeks after the surgery, mice that received surgery were further divided randomly into 3 groups: 1) untreated group (U); 2) low-dose TC group (L); 3) high-dose TC group (H). Group S received the same treatment as in group H. Two weeks after treatment, all mice were sacrificed and their ectopic endometrial tissues were harvested and analyzed by immunohistochemistry analysis. Hotplate test was administrated to all mice before the induction, treatment and sacrifice. Lesion size, hotplate latency, immunoreactivity against markers of proliferation, angiogenesis, H3K4 methylation, and of epithelial-mesenchymal transition (EMT). RESULTS: TC treatment significantly and substantially reduced the lesion size and improved generalized hyperalgesia in a dose-dependent fashion in mice with induced endometriosis. In addition, TC treatment resulted in reduced immunoreactivity to biomarkers of proliferation, angiogenesis, and H3K4 methylation, leading to arrested EMT and lesion growth. CONCLUSION: In light of our previously reported reduced cellular proliferation, cell cycle progression and invasiveness resulting from the LSD1 inhibition in in vitro studies, our data strongly suggest that LSD1 is a promising therapeutic target for endometriosis. TRIAL REGISTRATION: Not applicable.

My notes (saved in your browser only)

Condition tags

endometriosis

MeSH descriptors

Endometriosis Histone Demethylases Hyperalgesia Monoamine Oxidase Inhibitors Tranylcypromine Animals Biomarkers Biomarkers Cell Proliferation Cell Proliferation Endometriosis Female Histone Code Histone Code Histone Demethylases Histones Histones Hyperalgesia Immunohistochemistry Methylation

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (65)

Cited by (16)

Source provenance

europepmc
last seen: 2026-06-11T06:19:48.454388+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-05-13T22:21:07.355239+00:00
License: CC0 · commercial use OK