CHCHD2 Regulates Mitochondrial Function and Apoptosis of Ectopic Endometrial Stromal Cells in the Pathogenesis of Endometriosis

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AI-generated summary by claude@2026-06+body, 2026-06-06

CHCHD2 expression is increased in endometriosis tissues and its knockdown impairs mitochondrial function, reduces proliferation, and enhances apoptosis in ectopic stromal cells.

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AI-generated deep summary by claude@2026-06, 2026-06-06

The study examined CHCHD2 expression in ectopic and eutopic endometrium tissues from patients with endometriosis and compared it with normal endometrium, then used CHCHD2 knockdown in ectopic endometrial stromal cells to assess mitochondrial function/morphology, mitochondrial-mediated apoptosis, and proliferation and migration. CHCHD2 mRNA and protein levels were significantly increased in both eutopic and ectopic tissues, and its downregulation induced mitochondrial dysfunction marked by mitochondrial permeability transition pore opening, loss of mitochondrial membrane potential, cytochrome c release, and morphological damage, alongside reduced proliferation, decreased migration, and increased mitochondrial-mediated apoptosis. A key caveat is that the work relies on knockdown experiments in ectopic stromal cells rather than showing causality in vivo. This paper is centrally about endometriosis — it tests whether elevated CHCHD2 regulates mitochondrial dysfunction and apoptosis in ectopic endometrial stromal cells, contributing to endometriosis pathogenesis.

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Condition tags

endometriosis

MeSH descriptors

DNA-Binding Proteins DNA-Binding Proteins DNA-Binding Proteins Endometriosis Endometriosis Transcription Factors Transcription Factors Apoptosis Apoptosis Endometrium Endometrium Female Humans Mitochondria Mitochondria Stromal Cells Stromal Cells

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europepmc
last seen: 2026-06-16T06:07:01.518242+00:00
openalex
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pubmed
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