Pablo Hermida Lazcano on Muck Rack

Pablo Hermida Lazcano

As seen in: Nature, The Journal of Biological Chemistry
Is this you? As a journalist, you can create a free Muck Rack account to customize your profile, list your contact preferences, and upload a portfolio of your best work. Claim your profile

Get in touch with Pablo Hermida

Contact Pablo Hermida, search articles and posts on X, monitor coverage, and track replies from one place.

Learn more about Muck Rack

Actions

Share this page

Is this you?

As a journalist, you can create a free Muck Rack account to customize your profile, list your contact preferences, and upload a portfolio of your best work.
Claim your profile

Articles

Deep learning-based differential diagnosis of major depression and bipolar disorder using microglia-cellular sensors and patient-derived small extracellular vesicles

|
By Jorge Zambrano, Alejandro Luarte, Julian Grandvallet Contreras, Julián Esteban Contreras, Juan Perez, Juan Pérez Verified, Liliana Yantén-Fuentes, Miguel A. Prieto, Pablo Hermida Lazcano, Úrsula Wyneken, Claudio A. Perez
| Nature Verified
Abstract The diagnosis of major depressive disorder (MDD) and bipolar disorder (BD) relies on symptom-based evaluations. Both MDD as well as BD present episodes of depressed mood, often leading to misdiagnosis and treatment delays.
Open in Who Shared Issue with article?

Upregulation of the AMPK-FOXO1-PDK4 pathway is a primary mechanism of pyruvate dehydrogenase activity reduction and leads to increased glucose uptake in tafazzin-deficient cells

|
By Michael Schmidtke, Pablo Hermida Lazcano, Zhuqing Liang, Tyler Ralph-Epps
| biorxiv.org
Abstract Barth syndrome (BTHS) is a rare disorder caused by mutations in the TAFAZZIN gene. Previous studies from both patients and model systems have established metabolic dysregulation as a core component of BTHS pathology. In particular, features such as lactic acidosis, pyruvate dehydrogenase (PDH) deficiency, and aberrant fatty acid and glucose oxidation have been identified.
Open in Who Shared Issue with article?

Anomalous peroxidase activity of cytochrome c is the primary pathogenic target in Barth syndrome - Nature Metabolism

|
By Valerian E. Kagan, Yulia Y Tyurina, Alessia Lasorsa, Andrew A. Amoscato, Haider H. Dar, Pablo Hermida Lazcano, Michael Schmidtke, Pushpa Rampratap, Jeffrey Atkinson, Robert Wessells, Ivet Bahar, Hulya Bayir, Karolina Mikulska-Ruminska, Eduardo Vieira Neto, Svetlana N. Samovich, Austin B. Souryavong, Abu Ramim, Aybike Korkmaz, Georgy K. Vladimirov, Margarita A. Artyukhova
| Nature Verified
Abstract Barth syndrome (BTHS) is a life-threatening genetic disorder with unknown pathogenicity caused by mutations in TAFAZZIN (TAZ) that affect remodeling of mitochondrial cardiolipin (CL). TAZ deficiency leads to accumulation of mono-lyso-CL (MLCL), which forms a peroxidase complex with cytochrome c (cyt c) capable of oxidizing polyunsaturated fatty acid-containing lipids.
Open in Who Shared Issue with article?
See all 5 articles
 •  Privacy  •  Terms  •  Security and Legal  •   •   •   • 

© 2026 Muck Rack

SOC 2® Certified