Brett A. Kaufman

The paper examines the mRNA abundance of RIDD target genes in heart failure patients and mice, finding decreased expression consistent with RIDD activation.

This study shows that loss of TFAM in alveolar type 2 cells leads to mitochondrial dysfunction and fibrosis by promoting senescence and a profibrotic secretory program.

This study identifies QKI as a regulator of mitochondrial integrity in COPD, showing its protective role against emphysema through maintenance of mitochondrial function.

This study shows Adropin treatment reverses cardiac dysfunction and metabolic defects in a mouse model of HFpEF by reducing O-GlcNAcylation of LCAD and improving fatty acid oxidation.

This study shows that maternal extracellular vesicles from COVID-19 pregnancies alter trophoblast function, contributing to placental dysfunction.

This study identifies Gcn5l1 as a heart-specific factor that modulates cholesterol metabolism and heart-to-liver crosstalk in cardiometabolic heart failure, revealing the heart's role in systemic metabolic dysfunction.

This study shows that TCA cycle dysfunction and amino acid catabolism in mice with HFpEF drive hepatic steatosis similar to human NAFLD.

This paper shows that GDF15 levels rise with psychosocial stress, depression, anxiety, and biological aging, and that saliva GDF15 has a distinct diurnal pattern and responds rapidly to acute stress.

MitoQuicLy quantifies cf-mtDNA in plasma, serum, and saliva with high agreement to column-based methods, showing significant inter-individual and biofluid-specific differences.

This study generates a murine model of the human CREBRFR457Q obesity-risk variant and finds it does not affect energy or glucose homeostasis under various nutritional stress conditions.

This study shows psychological stress increases circulating cell-free mitochondrial DNA (ccf-mtDNA) in humans through glucocorticoid signaling, with no change in nuclear DNA levels.

This study shows that G-quadruplex structures in mtDNA regulate mitochondrial function, and RHPS4, a G4 ligand, affects mtDNA replication, transcription, and respiratory function in normal cells.

This study shows that small-molecule G-quadruplex binders can reduce pathogenic mtDNA heteroplasmy in fibroblasts, increasing complex I protein levels.