Short CV/Education and training

Present Positions

  • Since 2018
    Professor: Nanshan distinguish Professorship of outstanding talents (guest professorship), Department of Gynecology at the First Affiliated Hospital of Guangzhou Medical University, China

  • Since 2017
    Professor: Reproductive Physiology, Department of Physiology and Pharmacology, KI, Stockholm

Previous Positions and Periods of Appointment

  • 2015 – 2017
    Senior Lecturer, Department of Physiology and Pharmacology, KI

  • 2009 – 2015
    Researcher, Institute of Neuroscience and Physiology, Department of Physiology, GU

  • 2009 – 2016
    Professor (guest professorship): “Longjiang Scholar” at Heilongjiang University, Department of Obstetrics and Gynecology, Harbin, China

  • 2005 – 2008
    Junior researcher position at Swedish Research Council (VR) Institute of Neuroscience and Physiology, GU

  • 2000 – 2004
    Staff scientist at Department of Obstetrics and Gynecology, Wallenberg Laboratory, and lecturer at Department of Physiotherapy, GU

  • 1995 – 2000
    PhD student, Department of Obstetrics and Gynecology, GU

Docent level (Associate Professor)

  • Since 2004
    Associate professor (docent) 2004, GU and from 2015 at Karolinska Institutet (KI), Stockholm

Post Doctoral Position

  • 2002 – 2003
    Basic Medical Research Center, International University of Health and Welfare, Otawara, Japan, financed by The Swedish Foundation for International Cooperation in Research and Higher Education (STINT)

Doctoral Degree

  • 2000
    PhD in Obstetrics and Gynecology (Medical Science) at The Department of Obstetrics and Gynecology, Sahlgrenska Academy, University of Gothenburg (GU), Sweden (2000-11-03)

Selected publications

  • Stener-Victorin E, Deng Q. Epigenetic inheritance of polycystic ovary syndrome — challenges and opportunities for treatment. Nat Rev Endocrinol. 2021, July. Doi: 10.1038/s41574-021-00517-x

  • Stener-Victorin E, Deng Q. Transmission of Polycystic Ovary Syndrome via Epigenetic Inheritance. Trends Mol Med, 2021 Jun 11; pp. 1471-4914(21)00129-5. Doi:

  • Wu X-K*, Stener-Victorin E*, Kuang H-Y, Ma H-L, Gao J-S, Xie L-Z, Hou L-H, Hu Z-X, Shao X-G, Ge J, Zhang J-F, Xue H-Y, Xu X-F, Liang R-N, Ma H-X, Yang H-W, Li W-L, Huang D-M, Sun Y, Hao C-F, Du S-M, Yang Z-W, Wang X, Yan Y, Chen X-H, Fu P, Ding C-F, Gao Y-Q, Zhou Z-M, Wang CC, Wu T-X, Liu J-P, Ng EHY, Legro RS, Zhang H for PCOSAct Study. Acupuncture and Clomiphene for Infertility in the Polycystic Ovary Syndrome: A Randomized Clinical Trial. JAMA 2017 Jun 27; 317(24): 2502-2514. Doi: 10.1001/jama.2017.7217. PMID: 28655015. * Shared First Authors

  • Stener-Victorin E, Padmanabhan V, Walters KA, Campbell RE, Benrick A, Giacobini P, Dumesic DA, Abbott DA. Animal models to understand the etiology and pathophysiology of polycystic ovary syndrome. Endocrine Reviews. 2020; 41(4). Doi:

  • Risal S, Pei Y, Lu H, Manti M, Fornes R, Pui HP, Zhao Z, Massart J, Ohlsson C, Lindgren E, Crisosto N, Maliqueo M, Echiburú B, Ladrón de Guevara A, Sir-Petermann T, Larsson H, Rosenqvist MA, Cesta CE, Benrick A, Deng Q, Stener-Victorin E. Prenatal androgen exposure and transgenerational susceptibility to polycystic ovary syndrome. Nat Med. 2019; 25(12): 1894-1904. PMID: 31792459.

  • Manti M, Fornes R, Pironti G, McCann Haworth S, Zhengbing Z, Benrick A, Carlström M, Andersson D, Stener-Victorin E. Maternal androgen excess induces cardiac hypertrophy and left ventricular dysfunction in female mice offspring. Cardiovasc Res. 2019; 116(3): 619-632. PMID: 31382275.

  • Nilsson E, Benrick A, Kokosar M, Krook A, Lindgren E, Källman T, Martis MM, Højlund K, Ling C, Stener-Victorin E. Transcriptional and epigenetic changes influencing skeletal muscle metabolism in women with polycystic ovary syndrome. J Clin Endocrinol Metab. 2018;103(12): 4465-4477. Doi: 10.1210/jc.2018-00935.

  • Kokosar M, Benrick A, Perfilyev A, Nilsson E, Fornes R, Maliqueo M, Behre CJ, Sazonova A, Ohlsson C, Ling C, Stener-Victorin E. Epigenetic and transcriptional alterations in human adipose tissue of polycystic ovary syndrome. Scientific Report. 2016; 6: 22883. Doi: 10.1038/srep22883. PMID. 26975253.

  • Hu M, Richard JE, Maliqueo M, Kokosar M, Fornes R, Benrick A, Jansson T, Ohlsson C, Wu X, Skibicka KP, Stener-Victorin E. Maternal testosterone exposure increases anxiety-like behavior and impacts the limbic system in the offspring. Proc Natl Acad Sci USA. 2015; 112(46): 14348-53. PMID: 26578781.

  • Dumesic DA, Oberfield SE, Stener-Victorin E, Marshall JC, Laven JS, Legro RS. Scientific Statement on the Diagnostic Criteria, Epidemiology, Pathophysiology, and Molecular Genetics of Polycystic Ovary Syndrome. Endocr Rev. 2015 Oct;36(5): 487-525. Doi: 10.1210/er.2015-1018. PMID: 26426951.

  • Jedel E, Waern M, Gustafson D, Landen M, Eriksson E, Holm G, et al. Anxiety and depression symptoms in women with polycystic ovary syndrome compared with controls matched for body mass index. Hum Reprod. 2010 Feb; 25(2): 450-6.

  • Johansson J, Manneras-Holm L, Shao R, Olsson A, Lonn M, Billig H, et al. Electrical vs manual acupuncture stimulation in a rat model of polycystic ovary syndrome: different effects on muscle and fat tissue insulin signaling. PLoS One. 2013; 8(1): e54357.

  • Johansson J, Redman L, Veldhuis PP, Sazonova A, Labrie F, Holm G, et al. Acupuncture for ovulation induction in polycystic ovary syndrome: a randomized controlled trial. Am J Physiol Endocrinol Metab. 2013 May 1; 304(9): E934-43.

  • Johansson J, Yi F, Shao R, Lonn M, Billig H, Stener-Victorin E. Intense Acupuncture Normalizes Insulin Sensitivity, Increases Muscle GLUT4 Content, and Improves Lipid Profile in a Rat Model of Polycystic Ovary Syndrome. Am J Physiol Endocrinol Metab. 2010 Jul 27; 299: E551-E9.

  • Maliqueo M, Sun M, Johansson J, Benrick A, Labrie F, Svensson H, et al. Continuous administration of a P450 aromatase inhibitor induces polycystic ovary syndrome with a metabolic and endocrine phenotype in female rats at adult age. Endocrinology. 2013 Jan; 154(1): 434-45.

  • Manneras-Holm L, Baghaei F, Holm G, Janson PO, Ohlsson C, Lonn M, et al. Coagulation and fibrinolytic disturbances in women with polycystic ovary syndrome. J Clin Endocrinol Metab. 2011 Apr; 96(4): 1068-76.

Complete list of publications

Selected projects

  • Polycystic ovary syndrome (PCOS) is linked to reproductive and metabolic disturbances as well as to mental health conditions such as anxiety and depression. Our research aims to gain deeper understanding of the etiology and heritability of PCOS and associated comorbidities such as type 2 diabetes, endometrial dysfunction, and mental-health disorders across generations by dissecting the molecular, mechanistic, and causal links, and to determine whether men can also transmit the disease.

  • Delineate the roles of different androgen triggers and molecular pathways that drive transgenerational transmission of PCOS-like traits

    We know that hyperandrogenemia plays a key pathogenic role and that PCOS runs in families, with an estimated heritability of 70%. In a register-based study of nearly 30,000 daughters of women with or without PCOS, we found that daughters of women with PCOS have a five-fold increased risk of being diagnosed with the syndrome (Risal et al. Nature Medicine, 2019). But how PCOS is inherited remains unclear.

  • Accumulating evidence suggests that an epigenetic process triggered by an adverse maternal-fetal environment could yield the same phenotypic heritability as conventional genetics. Recently we made the discovery that PCOS-like traits induced by maternal androgen-exposure (Risal et al. Nature Medicine, 2019) can be passed on in mice from mothers (F0) to daughters (F1), granddaughters (F2), and even to great-granddaughters (F3), and that transcriptional and mitochondrial perturbations of oocytes accompany the transgenerational transmission. These intriguing findings raise the possibility that epigenetic modifications carried by germ cells and/or somatic cells can transmit PCOS across multiple generations. But they do not account for how males are affected and for the genetic contribution of the inheritance. Neither do these experiments disentangle the contribution of germ cells from that of the in utero environment in driving transgenerational transmission of PCOS.

  • Define cell-type-specific disease signatures in endometrium, adipose and skeletal muscle tissues

    Despite increasing evidence that multiple aspects of adipose tissue, skeletal muscle, and endometrial dysfunctions in women with PCOS are regulated by both genetic and epigenetic mechanisms, the contribution of cellular heterogeneity to these tissue dysfunctions is unclear. To gain insight into the cellular complexity and to tease apart genetic and epigenetic influence, we will characterize gene expression and DNA methylation at the single-cell level in endometrial, skeletal muscle and adipose tissues of women with and without the syndrome.

  • Establishment of endometrial organoids and adipocyte spheroids

    Endometrial organoids (EOs) and adipocyte spheroids (ASs) circumvent constraints associated with fresh tissue and are unique powerful tools for pathophysiological research, functional testing of cell-type-specific disease markers, and drug screening of novel therapeutic targets. We establish EOs of endometrial tissue and ASs of adipose tissue (in collaboration with Carolina Hagberg, KI) of women with PCOS and controls. These will be used to test how e.g. sex steroids and/or insulin affect altered signaling pathways identified by cell-type specific large-scale sequencing.

  • To elucidate the effect and mechanisms of metformin and acupuncture on insulin resistance and key signaling pathways in target tissues in women with PCOS

    Prevention of PCOS is limited and management inadequate due to lack of mechanistic insights of PCOS. Changes in diet and lifestyle is the first choice for improving insulin sensitivity and preventing type 2 diabetes. Metformin is used in those with impaired glucose tolerance and type 2 diabetes who do not respond to lifestyle changes and works mainly by reducing hepatic gluconeogenesis and to a lesser extent by increasing glucose uptake in skeletal muscle and adipose tissue. An alternative approach to metformin and exercise is electroacupuncture treatment. We have in an uncontrolled study showed that repeated low-frequency electroacupuncture improves insulin sensitivity, decreases excess androgen levels, and restores altered epigenetic and transcriptional changes in adipose tissue and that the effect is mediated by neuronal circuits in the sympathetic and endocrine system. Moreover, our recent findings provide evidence that a single bout of electroacupuncture normalizes gene expression in skeletal muscle in a manner like acute exercise. Electroacupuncture might therefore be a useful way of assisting those who have difficulties performing exercise. In an on-going randomized control (RCT) (NCT01457209) we investigate the effectiveness of metformin, low-frequency electroacupuncture, and lifestyle management for improving insulin sensitivity in women with PCOS. Moreover, we explore whether these treatments can remodel transcriptional changes and restore molecular dysfunctions and in endometrium, adipose tissue and skeletal muscle tissue biopsies at baseline, after 16 weeks of treatment and at follow up to advance our understanding of PCOS-specific insulin resistance.

  • Determine the role of the immune system in the pathology of PCOS

    Women with PCOS suffer from chronic low-grade inflammation and some even develop autoimmune diseases, which are further aggravated by metabolic disturbances that characterize the syndrome. Accumulating evidence suggests a link between PCOS and immune responses, but whether the observed immune hyperactivation is a cause or consequence of hyperandrogenism, and whether this immunophenotype is passed on to subsequent generations is unknown. To investigate what role the immune system play in the pathology of PCOS we currently investigate whether:

    1. Transfer of self-reactive IgG from women with PCOS to mice induce a PCOS-like phenotype?

    2. Characterize immunophenotype in androgen-induced PCOS mice.

    3. Determine whether transferring B cells from androgen-induced PCOS mice to reconstituted B-null mice induces development of a PCOS-like immunophenotype.

Membership in scientific bodies/juries

  • Endocrine Society

  • European Society of Endocrinology

  • European Society of Human Reproduction and Embryology

  • European Association for the Study of Diabetes

  • Scandinavian Society for the Study of Diabetes

Grant Reviewer

  • Swedish Research Council, Panel B1: Endocrinology and Metabolism

  • Medical Research council (MRC), 5 years MRC grants, UK. Wellbeing of Women Research Grant 2011, UK

  • Health Research Council of New Zealand (HRC), 3 years HRC grants, New Zealand

Editorial Board

  • Associate Editor: Human Reproduction, since 2013

  • Associate Editor: Acupuncture in Medicine, BMJ group, since 2010

Media coverage

Soft Skills/Other activities and achievements

Other activities and achievements/family

  • Family situation: married to Hans Victorin; two children: Maja (born in 1991) and Jacob (born in 1994)

  • Activities: kitesurfing, skiing and sailing

  • Other activities: I regularly lecture at different levels at Karolinska Institutet, Stockholm, Sweden and within the health care system. Thus, I teach medical-, pharmacy-, and physiotherapy/occupational therapy students at undergraduate, graduate, and postgraduate level with physiology as the main subject; endocrinology, autonomic nervous system, exercise physiology, neurophysiology with main focus on pain physiology and sensory stimulation.


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