Sara Windahl

Assistant Senior Lecturer

Karolinska Institutet-Huddinge Campus

Sweden

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Sara Windahl is an Assistant Senior Lecturer at Karolinska Institutet - Huddinge Campus, Sweden. Her research focuses on bone biology, particularly the mechanisms of osteoclast differentiation, sex-specific responses to hormonal treatments, and the skeletal effects of mechanical loading. Recent publications include studies on the role of tartrate-resistant acid phosphatase in bone mass regulation and the influence of estrogen on skeletal responses in male mice.

Articles (11)

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2024

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2023

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2023

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2022

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2022

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2022

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2022

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2020

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2020

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2020

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2020

Collaborators (11)

Klara Sjögren

University of Gothenburg

SWEDEN

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Marie Lagerquist

Associate Professor

University of Gothenburg

SWEDEN

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Hannah Colldén

University of Gothenburg

SWEDEN

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Audrey S Chan

University of Melbourne

AUSTRALIA

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Cecilia Engdahl

SWEDEN

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Liesbeth Vandenput

Professor

Australian Catholic University

AUSTRALIA

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Matti Poutanen

professor

FINLAND

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Natalie A Sims

AUSTRALIA

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Claes Ohlsson

University of Gothenburg

SWEDEN

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Jasmine Samvelyan

Senior Lecturer in Biomedical Science

UNITED KINGDOM

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Petra Henning

University of Gothenburg

SWEDEN

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Sara Windahl

Research Interests

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About

Articles (11)

Tartrate-resistant acid phosphatase (TRAP/ACP5) promotes bone length, regulates cortical and trabecular bone mass, and maintenance growth plate architecture and width in a sex- and site-specific manner in mice

RANKL-dependent osteoclast differentiation and gene expression in bone marrow-derived cells from adult mice is sexually dimorphic

A COX‐2 Inhibitor Does Not Interfere With the Bone‐Protective Effects of Loading in Male Mice With Arthritis

Phosphorylation of S122 in ERα is important for the skeletal response to estrogen treatment in male mice

Dehydroepiandrosterone Supplementation Results in Varying Tissue-specific Levels of Dihydrotestosterone in Male Mice

Comprehensive Sex Steroid Profiling in Multiple Tissues Reveals Novel Insights in Sex Steroid Distribution in Male Mice

STAT3 Hyperactivation Due to SOCS3 Deletion in Murine Osteocytes Accentuates Responses to Exercise‐ and Load‐Induced Bone Formation

The effects of estradiol are modulated in a tissue-specific manner in mice with inducible inactivation of ERα after sexual maturation

Bone gain following loading is site-specifically enhanced by prior and concurrent disuse in aged male mice

αSMA Osteoprogenitor Cells Contribute to the Increase in Osteoblast Numbers in Response to Mechanical Loading

Changes in mechanical loading affect arthritis-induced bone loss in mice

Collaborators (11)

Klara Sjögren

Marie Lagerquist

Hannah Colldén

Audrey S Chan

Cecilia Engdahl

Liesbeth Vandenput

Matti Poutanen

Natalie A Sims

Claes Ohlsson

Jasmine Samvelyan

Petra Henning

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