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Neuroinflammaging, a moderate, chronic, and sterile inflammation in the hippocampus, contributes to age-related cognitive decline. Neuroinflammaging comprises the activation of the nucleotide-binding...

Earth-based hiPSC models have transformed disease research but remain limited by cellular immaturity, a strong reliance on glycolysis rather than oxidative phosphorylation (OXPHOS), and incomplete tissue architecture. Animal models often fail to recapitulate human phenotypes, and primary patient tissues are difficult to obtain, especially for rare pediatric conditions. Spaceflight exposes cells to microgravity and space radiation, stress conditions that may unmask or amplify disease-relevant vulnerabilities. Because these stressors converge on mitochondrial and cardiac pathways, they offer a biologically distinct context for studying rare metabolic and congenital disorders. Conventional culture also differs in oxygen tension. Based on these challenges, deeper investigation is needed into how patient-derived human induced pluripotent stem cells (hiPSCs) models respond to the space environment. A review published (DOI: 10.1093/pcmedi/pbag028) in Precision Clinical Medicine in 2026 by researchers affiliated with IRCCS Policlinico San Donato, the University of Milan, and Weill Cornell Medicine, with collaborators from multiple institutions, examines current space-based hiPSC studies and their relevance to mitochondrial diseases and congenital heart disorders (CHDs), and their potential to inform rare pediatric disease research. It summarizes reported effects on mitochondrial function, cytoskeletal organization, oxidative stress, calcium handling, and gene expression, and outlines experimental and mechanistic gaps that must be addressed...

Newswise — Earth-based hiPSC models have transformed disease research but remain limited by cellular immaturity, a strong reliance on glycolysis rather than oxidative phosphorylation (OXPHOS), and incomplete tissue architecture. Animal models often fail to recapitulate human phenotypes, and primary patient tissues are difficult to obtain, especially for rare pediatric conditions. Spaceflight exposes cells to microgravity and space radiation, stress conditions that may unmask or amplify disease-relevant vulnerabilities. Because these stressors converge on mitochondrial and cardiac pathways, they offer a biologically distinct context for studying rare metabolic and congenital disorders. Conventional culture also differs in oxygen tension. Based on these challenges, deeper investigation is needed into how patient-derived human induced pluripotent stem cells (hiPSCs) models respond to the space environment. A review published (DOI: 10.1093/pcmedi/pbag028) in Precision Clinical Medicine in 2026 by researchers affiliated with IRCCS Policlinico San Donato, the University of Milan, and Weill Cornell Medicine, with collaborators from multiple institutions, examines current space-based hiPSC studies and their relevance to mitochondrial diseases and congenital heart disorders (CHDs), and their potential to inform rare pediatric disease research. It summarizes reported effects on mitochondrial function, cytoskeletal organization, oxidative stress, calcium handling, and gene expression, and outlines experimental and mechanistic gaps that must...

Funded 4-year EASTBIO PhD at Dundee: map how SRPK kinase signalling drives Alzheimer's using phosphoproteomics in hiPSC neurons and brain tissue.

Read the full paper: Generation of inducible LMNA and Progerin hiPSC lines for controlled modelling of cellular ageing

Read the full paper: Combinatorial and Inducible CRISPRa/i Enables Canalized hiPSC Forward Programming and Iterative Refinement via Single-Cell Genomics

Generating mature human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) remains a major obstacle to accurate disease modeling and cardiac repair. As the transcription factor Irx3 is a key determinant of ventricular conduction system fate in mice, we hypothesized that suppressing IRX3 expression accelerates human working cardiomyocyte differentiation. Here, we demonstrate that depleting IRX3 enhances hiPSC-CM differentiation. IRX3-knockout (KO) hiPSCs generated a greater number of cardiomyocytes with elevated expression of TNNI1 and CX43. Notably, IRX3-KO cardiomyocytes exhibited improved electrophysiological properties, more uniform mitochondrial distribution, better sarcomere organization, and enhanced intercellular connectivity. We observed that IRX3 expression peaks during the early stages of cardiomyocyte differentiation, whereas IRX3-KO cardiac progenitors have increased expression of GATA4, NKX2–5, and TBX5, as well as enhanced cell proliferation. These int

Hundreds of mutations to the broadly expressed LMNA gene cause disease primarily within cardiac, muscular, and adipose tissues¹. Tissue-specific pathogenesis arises when mutant protein dysfunction collides with the unique demands of a specific cell type. Here, we decipher the cell-type-specific consequences of ~15,000 LMNA mutations by completing the first saturation mutagenesis screens in human induced pluripotent cells (hiPSCs) and hiPSC-derived cardiomyocytes using our newly developed single...