Linus Shao

MD, PhD, Associate Professor

University of Gothenburg, Sahlgrenska Academy

Sweden

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Linus Shao, MD, PhD, is an Associate Professor at The Sahlgrenska Academy at the University of Gothenburg, Sweden. His research primarily focuses on polycystic ovary syndrome (PCOS), investigating areas such as uterine inflammation, insulin resistance, and placental senescence. Recent publications highlight his work on the interplay between androgen levels and related metabolic disorders in pregnancy.

Articles (10)

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2023

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2023

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2022

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2021

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2021

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2021

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2021

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2021

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2021

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2020

Collaborators (2)

Amanda Sferruzzi-Perri

University Lecturer in Reproductive Physiology (proleptic appointment)

University of Cambridge

UNITED KINGDOM

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Juan Ignacio Rodriguez

Karolinska Institutet

SWEDEN

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Linus Shao

Research Interests

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Articles (10)

Defective Uterine Spiral Artery Remodeling and Placental Senescence in a Pregnant Rat Model of Polycystic Ovary Syndrome

Regulatory mechanisms of HMGB1 and its receptors in polycystic ovary syndrome‐driven gravid uterine inflammation

Overactivation of the androgen receptor exacerbates gravid uterine ferroptosis via interaction with and suppression of the NRF2 defense signaling pathway

TLR4-Associated IRF-7 and NFκB Signaling Act as a Molecular Link Between Androgen and Metformin Activities and Cytokine Synthesis in the PCOS Endometrium

Long-term androgen excess induces insulin resistance and non-alcoholic fatty liver disease in PCOS-like rats.

Long-term androgen excess induces insulin resistance and non-alcoholic fatty liver disease in PCOS-like rats

Increased uterine androgen receptor protein abundance results in implantation and mitochondrial defects in pregnant rats with hyperandrogenism and insulin resistance

Long-term androgen-induced nonalcoholic fatty liver disease in a polycystic ovary syndrome mouse model is related to mitochondrial dysfunction

Suppression of uterine and placental ferroptosis by N-acetylcysteine in a rat model of polycystic ovary syndrome

Cranial irradiation alters neuroinflammation and neural proliferation in the pituitary gland and induces late‐onset hormone deficiency

Collaborators (2)

Amanda Sferruzzi-Perri

Juan Ignacio Rodriguez

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