Marco António Campinho is an Invited Auxiliary Professor at the Faculty of Medicine and Biomedical Sciences, Universidade do Algarve, and Principal Investigator of the Thyroid Hormones in Development and Ageing group at the Algarve Biomedical Centre–Research Institute (ABC-Ri).
As an educator, he coordinates and lectures in Embryonic Development Biology, Bioinformatics, and Oncology Lab courses, and tutors Problem-Based Learning sessions in the Master of Medicine. He has supervised five PhD and six MSc students to completion, and serves as Vice-Director of ABC-Ri.
His research deploys zebrafish biomedical models to unravel the molecular and cellular mechanisms of thyroid hormone signalling in vertebrate development, with translational focus on rare neurodevelopmental disorders such as Allan-Herndon-Dudley Syndrome. He has authored 43 peer-reviewed publications (h-index 20), secured over €1.28 million in competitive funding, and edited six Frontiers eBooks.
The lab is composed of 1 PhD student, 2 Master Student, 2 BSc students and 1 PI.
The Thyroid Hormones in Development and Ageing group, led by Marco António Campinho at the Algarve Biomedical Centre–Research Institute (ABC-Ri), Universidade do Algarve, investigates the molecular and cellular mechanisms by which thyroid hormones (TH) regulate vertebrate development, using zebrafish as its primary biomedical model.
The group's central focus is on maternal thyroid hormones (MTH) as master regulators of early development. Key findings include the first demonstration that MTH are essential for zebrafish brain and spinal cord development, acting as cell fate determinants for neuronal and glial progenitors. Landmark work established the first vertebrate model of Allan-Herndon-Dudley Syndrome (AHDS), a rare human neurodevelopmental disorder, revealing that impaired MTH signalling reduces neural cell diversity and disrupts hindbrain vascularisation via a MTH–pax6a–VEGFAA axis. The group also uncovered how TH-dependent asymmetric ossification drives eye migration during flatfish metamorphosis, and how environmental endocrine disruptors (ioxynil, diethylstilbestrol) compromise thyroid and cardiovascular function at sub-threshold concentrations.
By bridging basic zebrafish developmental biology with human rare disease genetics, the group is fundamentally reshaped understanding of when and how TH acts during embryogenesis, opening new avenues for therapeutic target identification in TH-linked neurodevelopmental pathologies.
Transgenics
OMICS
CRISPR/Cas9 gene editing
High-resolution microscopy
Collaborations in Portugal (FCT-NOVA), Spain (CSIC-UIM, CSIC-Alberto Sols), Norway (Nord University) and Japan (NIG).
Trindade, M., Silva, N., Rodrigues, J., Kawakami, K., Campinho, M.A.*, 2025. Maternal thyroid hormone is required to develop the hindbrain vasculature in zebrafish. NPJ Communications Biology, 8, 960 (2025).
Silva, N. and Campinho, M.A*, 2023. In a zebrafish biomedical model of human Allan-Herndon-Dudley syndrome, impaired MTH signaling leads to decreased neural cell diversity. Frontiers in Endocrinology, Volume 14. https://www.frontiersin.org/articles/10.3389/fendo.2023.1157685
Li, Y.-F., Rodrigues, J., and Campinho, M.A.*, 2022. Ioxynil and diethylstilbestrol increase the risks of cardiovascular and thyroid dysfunction in zebrafish—Science of The Total Environment 838, 156386. https://doi.org/10.1016/j.scitotenv.2022.156386
Silva, N., Louro, B., Trindade, M., Power, D. M., Campinho, M. A.*, 2017. Transcriptomics reveal an integrative role for maternal thyroid hormones during zebrafish embryogenesis. NPJ Scientific Reports. 7, 16657.
Campinho, M. A., Saraiva, J., Florindo, C., Power, D. M., 2014. Maternal thyroid hormones are essential for neural development in zebrafish. Molecular Endocrinology. 28, 1136-1144.