The Impact of Mitochondrial Dysfunction in human oocytes on Embryo quality and Conception rates in IVF patients with varying stages of Endometriosis

In: American Journal of Medical and Clinical Research & Reviews · 2025 · vol. 04(03) · doi:10.58372/2835-6276.1270 · W4408546459
article OA: hybrid CC0
AI-generated summary by gemini-2.5-flash-lite, 2026-06-09

This study found that mitochondrial dysfunction, indicated by lower ATP and mtDNA deletions, negatively impacts oocyte quality and IVF success in women with endometriosis.

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, 2026-06-09 · read from full text

This prospective cohort study (2021–2024) examined 60 IVF patients aged 20–40 with either endometriosis (n=42) or no endometriosis (n=42) and assessed mitochondrial function in retrieved oocytes, measuring ATP content and mitochondrial DNA (mtDNA) integrity alongside oocyte maturation, fertilization, embryo development, implantation, and clinical pregnancy. The study found that endometriosis patients had lower oocyte ATP content and fewer mitochondria, particularly at prophase I and metaphase I, while mtDNA deletions were associated with worse oocyte quality and IVF success; all IVF cycles involving oocytes with mtDNA deletions resulted in failure. Although clinical pregnancy rates were similar between groups, live birth rates were slightly lower in the endometriosis group, and demographic/clinical differences (e.g., age, BMI, FSH, infertility duration) were noted as potential confounders. This paper is centrally about endometriosis — it directly links mitochondrial dysfunction in human oocytes (ATP reduction and mtDNA deletions) to IVF embryo quality and conception/live birth outcomes across stages of endometriosis.

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

Abstract

Background: Endometriosis is a chronic, estrogen-dependent gynecological condition that is closely linked to infertility. Although significant progress has been made in assisted reproductive technologies (ART), including in vitro fertilization (IVF), women with endometriosis frequently encounter challenges such as poor oocyte quality, impaired embryo development, and lower pregnancy rates. Emerging evidence suggests that mitochondrial dysfunction, particularly through reduced ATP production and mitochondrial DNA (mtDNA) deletions, plays a critical role in the reproductive difficulties observed in these patients. Aim: The aim is to evaluate the impact of mitochondrial dysfunction on oocyte quality, embryo development, and IVF outcomes in women with endometriosis, comparing them with a control group of women without endometriosis. Methodology: A prospective cohort study was conducted over three years (2021-2024) at the Medical Health and Research Institute, involving 60 women aged 20-40 years. The cohort consisted of 42 women diagnosed with endometriosis (study group) and 42 women undergoing IVF treatment without endometriosis (control group). Mitochondrial function, including ATP content and mitochondrial DNA (mtDNA) integrity, was assessed in oocytes retrieved from both groups. The study compared the outcomes of oocyte maturation, fertilization rates, embryo development, implantation rates, and clinical pregnancy between the two groups. Results: The demographic and clinical characteristics of patients with endometriosis and controls revealed significant differences in age, body mass index (BMI), follicle-stimulating hormone (FSH) levels, and infertility duration. IVF outcomes showed no significant difference in clinical pregnancy rates (54.7% in endometriosis patients vs. 52.3% in controls), but endometriosis patients had slightly lower live birth rates (45.2% vs. 52.3%). Oocyte quality analysis indicated that endometriosis patients exhibited lower ATP content and mitochondrial number, particularly at the prophase I (PI) and metaphase I (MI) stages. Mitochondrial DNA deletions were found to have a significant negative impact on oocyte quality and IVF success, with all cycles involving oocytes with mtDNA deletions resulting in failure, including a biochemical pregnancy in a patient with moderate endometriosis. Conclusion: Mitochondrial dysfunction, characterized by reduced ATP levels and mtDNA deletions, adversely impacts oocyte quality and IVF outcomes in women with endometriosis. These results highlight the importance of personalized IVF protocols that focus on mitochondrial health, potentially enhancing reproductive outcomes. Further research is needed to explore targeted interventions to minimize mitochondrial damage and improve ART success in this population.
Full text 7,755 characters · extracted from oa-doi-fallback · 4 sections · click to expand

Background

Endometriosis is a chronic, estrogen-dependent gynecological condition that is closely linked to infertility. Although significant progress has been made in assisted reproductive technologies (ART), including in vitro fertilization (IVF), women with endometriosis frequently encounter challenges such as poor oocyte quality, impaired embryo development, and lower pregnancy rates. Emerging evidence suggests that mitochondrial dysfunction, particularly through reduced ATP production and mitochondrial DNA (mtDNA) deletions, plays a critical role in the reproductive difficulties observed in these patients. Aim: The aim is to evaluate the impact of mitochondrial dysfunction on oocyte quality, embryo development, and IVF outcomes in women with endometriosis, comparing them with a control group of women without endometriosis. Methodology: A prospective cohort study was conducted over three years (2021-2024) at the Medical Health and Research Institute, involving 60 women aged 20-40 years. The cohort consisted of 42 women diagnosed with endometriosis (study group) and 42 women undergoing IVF treatment without endometriosis (control group). Mitochondrial function, including ATP content and mitochondrial DNA (mtDNA) integrity, was assessed in oocytes retrieved from both groups. The study compared the outcomes of oocyte maturation, fertilization rates, embryo development, implantation rates, and clinical pregnancy between the two groups.

Results

The demographic and clinical characteristics of patients with endometriosis and controls revealed significant differences in age, body mass index (BMI), follicle-stimulating hormone (FSH) levels, and infertility duration. IVF outcomes showed no significant difference in clinical pregnancy rates (54.7% in endometriosis patients vs. 52.3% in controls), but endometriosis patients had slightly lower live birth rates (45.2% vs. 52.3%). Oocyte quality analysis indicated that endometriosis patients exhibited lower ATP content and mitochondrial number, particularly at the prophase I (PI) and metaphase I (MI) stages. Mitochondrial DNA deletions were found to have a significant negative impact on oocyte quality and IVF success, with all cycles involving oocytes with mtDNA deletions resulting in failure, including a biochemical pregnancy in a patient with moderate endometriosis.

Conclusion

Mitochondrial dysfunction, characterized by reduced ATP levels and mtDNA deletions, adversely impacts oocyte quality and IVF outcomes in women with endometriosis. These results highlight the importance of personalized IVF protocols that focus on mitochondrial health, potentially enhancing reproductive outcomes. Further research is needed to explore targeted interventions to minimize mitochondrial damage and improve ART success in this population.

References

Assaf L, Eid AA, Nassif J. Role of AMPK/mTOR, mitochondria, and ROS in the pathogenesis of endometriosis. Life sciences. 2022 Oct 1;306:120805. Burney RO, Giudice LC. Pathogenesis and pathophysiology of endometriosis. Fertility and sterility. 2012 Sep 1;98(3):511-9. Bhurke AV, Das Mahapatra P, Balakrishnan S, Khan SA, et al. Clinical characteristics and surgical management of endometriosis‐associated infertility: A multicenter prospective cohort study. Int J Gynaecol Obstet. 2022 Oct;159(1):86-96. Cacciottola L, Donnez J, Dolmans MM. Can endometriosis-related oxidative stress pave the way for new treatment targets? Int. J. Mol. Sci. 2021 Jul 1;22(13):7138. Chapron C, Marcellin L, Borghese B, et al. Rethinking mechanisms, diagnosis and management of endometriosis. Nature Reviews Endocrinology. 2019 Nov;15(11):666-82. Cecchino GN, Seli E, da Motta EL, et al. The role of mitochondrial activity in female fertility and assisted reproductive technologies: overview and current insights. Reproductive biomedicine online. 2018 Jun 1;36(6):686-97. Demain LA, Conway GS, Newman WG. Genetics of mitochondrial dysfunction and infertility. Clin Genet 2017: 91: 199–207. Ferrero S, Anserini P, Remorgida V, et al. Body mass index in endometriosis. European Journal of Obstetrics & Gynecology and Reproductive Biology. 2005 Jul 1;121(1):94-8. Giudice LC, Kao LC. Theories of pathogenesis. Lancet. 2004;364:1789-99. Giudice LC. Clinical practice: endometriosis. The N Engl J Med. 2010 June 24; 362(25): 2389–2398. Hamdan M, Dunselman G, Li TC, et al. The impact of endometrioma on IVF/ICSI outcomes: a systematic review and meta-analysis. Human reproduction update. 2015 Nov 1;21(6):809-25. Hsu AL, Townsend PM, Oehninger S, et al. Endometriosis may be associated with mitochondrial dysfunction in cumulus cells from subjects undergoing in vitro fertilization-intracytoplasmic sperm injection, as reflected by decreased adenosine triphosphate production. Fertility and Sterility. 2015 Feb 1;103(2):347-52. Jenabi E, Khazaei S, Veisani Y. The association between body mass index and the risk of endometriosis: a meta-analysis. Journal of Endometriosis and Pelvic Pain Disorders. 2019 Jun;11(2):55-61. Kirillova A, Smitz JE, Sukhikh GT, et al. The role of mitochondria in oocyte maturation. Cells. 2021 Sep 19;10(9):2484. Latif S, Saridogan E. Endometriosis, Oocyte, and Embryo Quality.J. Clin. Med. 2023, 12, 4186 Macer ML, Taylor HS. Endometriosis and infertility: a review of the pathogenesis and treatment of endometriosis-associated infertility. Obstet Gynecol Clin North Am. 2012 December ; 39(4): 535–549. Máté G, Bernstein LR, Török AL. Endometriosis is a cause of infertility. Does reactive oxygen damage to gametes and embryos play a key role in the pathogenesis of infertility caused by endometriosis?. Frontiers in endocrinology. 2018 Nov 29;9:725. Nisenblat V, Bossuyt PM, Shaikh R, et al. Cochrane Gynaecology and Fertility Group. Blood biomarkers for the non‐invasive diagnosis of endometriosis. Cochrane Database Syst Rev 2016 May 1;2016(5):CD012179. Somigliana E, Berlanda N, Benaglia L, et al. Surgical excision of endometriomas and ovarian reserve: a systematic review on serum antimüllerian hormone level modifications. Fertility and sterility. 2012 Dec 1;98(6):1531-8. Somigliana E, Infantino M, Benedetti F, et al. The presence of ovarian endometriomas is associated with a reduced responsiveness to gonadotropins. Fertility and sterility. 2006 Jul 1;86(1):192-6. Torre SD, Benedusi V, Fontana R, et al. Energy metabolism and fertility—a balance preserved for female health. Nat. Rev. Endocrinol. 2014 Jan;10(1):13-23. Uncu G, Kasapoglu I, Ozerkan K, et al. Prospective assessment of the impact of endometriomas and their removal on ovarian reserve and determinants of the rate of decline in ovarian reserve. Human reproduction. 2013 Aug 1;28(8):2140-5. Van Blerkom J. Mitochondrial function in the human oocyte and embryo and their role in developmental competence. Mitochondrion. 2011 Sep 1;11(5):797-813. Wallace DC. Mitochondrial DNA mutations in disease and aging. Environmental and molecular mutagenesis. 2010 Jun;51(5):440-50. Zhang D, Keilty D, Zhang ZF, Chian RC. Mitochondria in oocyte aging: current understanding. Facts Views Vis Obgyn, 2017, 9 (1): 29-38 Zondervan KT, Becker CM, Missmer SA. Endometriosis. N Engl J Med. 2020 Mar 26;382(13):1244-1256. Downloads Published How to Cite Issue Section License Copyright (c) 2025 American Journal of Medical and Clinical Research & Reviews This work is licensed under a Creative Commons Attribution 4.0 International License.

Text is read by the "Ask this paper" AI Q&A widget below. Extraction quality varies by source — PMC NXML preserves structure cleanly, OA-HTML may include some navigation residue, and OA-PDF can have broken hyphenation. The publisher copy (via DOI) is the canonical version.

My notes (saved in your browser only)

Ask this paper AI returns verbatim quotes from the full text · source: oa-doi-fallback

Answers must be backed by verbatim quotes from this paper's full text. Hallucinated quotes are dropped automatically; if no verbatim passage answers the question, we say so. How this works

Condition tags

endometriosisinfertility

Citation neighborhood (no data yet)

We don't have any in-corpus citations linked to this paper yet. This is a recent paper (2025) — citers typically take a year or two to land, and the OpenAlex reference graph may still be filling in.

Source provenance

openalex
last seen: 2026-06-04T00:00:01.174412+00:00
License: CC0 · commercial use OK