Marlena Fejzo’s groundbreaking work implicates the hormone GDF15 as a key player in this understudied disorder.

Anxiety-like behaviour in mice, as a result of psychological stress, is shown to be mediated by GDF15 release in response to adipose tissue lipolysis.

The Growth Differentiation Factor 15 GDF15 Elisa Kit Market is expected to grow from 505.9 USD Million in 2025 to 1,200 USD Million by 2035. The Growth Differentiation Factor 15 GDF15 Elisa Kit Market...

Marlena Fejzo’s groundbreaking work implicates the hormone GDF15 as a key player in this understudied disorder.

Anxiety-like behaviour in mice, as a result of psychological stress, is shown to be mediated by GDF15 release in response to adipose tissue lipolysis.

A blood protein measured in midlife may predict future dementia risk and reveal immune pathways tied to vascular brain damage.

Breit and Tsai provide a concise overview of the role of GDF15 as a signalling molecule in the context of metabolic health and disease.

Those under 55 with relatively high levels of the molecule GDF15 had an elevated risk of developing dementia.

Those under 55 with relatively high levels of the molecule GDF15 had an elevated risk of developing dementia.

Anxiety-like behaviour in mice, as a result of psychological stress, is shown to be mediated by GDF15 release in response to adipose tissue lipolysis.

Anxiety-like behaviour in mice, as a result of psychological stress, is shown to be mediated by GDF15 release in response to adipose tissue lipolysis.

Cell Death Discovery - Variant-divergent death: Omicron intensifies bystander T-cell apoptosis via GDF15–BCL2L13

Khetarpal et al. show that the metabolic regulator PGC-1α is essential in heart muscle cells for exercise-driven cardiac growth, and that suppression of the stress-induced myokine GDF15 is required to enable cardiomyocyte adaptations to training.

Severe Omicron cases present profound lymphocytopenia, suggesting variant-specific immune injury. We identify CD63 as a conserved T-cell host factor supporting ACE2-independent SARS-CoV-2 entry. Despite lower intracellular viral loads than the ancestral strain, Omicron elicits enhanced T-cell apoptosis largely through a bystander mechanism. Omicron-stimulated epithelial cells secrete GDF15, which upregulates the pro-apoptotic protein BCL2L13 in T cells and thereby remotely accelerates apoptosis in uninfected bystanders. Functionally, recombinant GDF15 increases BCL2L13 and apoptosis, while genetic dampening of BCL2L13 blunts Omicron-specific high-intensity bystander death. In clinical samples, plasma GDF15 associates with mortality, SOFA scores, and lower lymphocyte counts, bridging the epithelial–immune axis to patient outcomes. Our data delineate a two-track model of Omicron immune injury—CD63-enabled T-cell entry plus GDF15–BCL2L13-driven bystander apoptosis—that reconciles lower epithelial cytopathicity with deeper T-cell depletion in critical disease. These findings nominate the GDF15–BCL2L13 axis as a mechanistic marker and potential point of intervention.

Cell Death Discovery - Variant-divergent death: Omicron intensifies bystander T-cell apoptosis via GDF15–BCL2L13