Orian S. Shirihai

The paper screens FDA-approved compounds to find mitophagy activators, identifying Meptazinol and Ponatinib as top candidates that increase mitolysosomes but do not rescue bioenergetic defects in mitochondrial diseases.

This study shows that targeting lysosomal pH with rapamycin or acidic nanoparticles restores mitochondrial function in GBA1-mutant Parkinson's disease neurons.

This paper shows that activating the MasR receptor with CAP-1902 improves mitochondrial function in a human Complex III deficiency model by enhancing turnover and reducing stress.

This study shows that UCP1-deficient mice adapt to cold by increasing mitochondrial calcium uptake via MCU, enhancing thermogenesis without UCP1.

This paper introduces GRID, a high-throughput image analysis method using dispersion indices to quantify subcellular structure dynamics and spatial distributions across diverse biological contexts.

This study shows the malate aspartate shuttle supports lipid mobilization in brown adipocytes by regulating lipid homeostasis and thermogenesis.

This study shows STX4 is essential for mitochondrial homeostasis in skeletal muscle by regulating mitochondrial biogenesis and mitophagy.

This study shows TRAF6 regulates glucose homeostasis via mitophagy in islets, with both Parkin-dependent and -independent pathways involved.

This study identifies SIRT2 as a regulator of β-cell proliferation, showing its role in controlling β-cell expansion during hyperglycemia while preserving feedback mechanisms.

The paper identifies impaired AMPK signaling in AT2 cells as a driver of pulmonary fibrosis and shows restoring AMPK alleviates fibrosis in vivo.

The paper identifies LPCAT3 as a cold-regulated enzyme that generates AA-PE in BAT mitochondria, enhancing ETC efficiency and thermogenesis.

The paper creates a brain-wide map of mitochondrial phenotypes by combining physical voxelization with biochemical profiling, revealing regional differences in mitochondrial density and function.

This study shows that reduced oxidative phosphorylation is not required for pro-inflammatory macrophage activation, challenging the conventional model of mitochondrial reprogramming.

This study identifies Mfn2's role in promoting NCLX-mediated Ca2+ release from mitochondria, linking mitochondrial ROS to mitophagy via Ca2+ signaling.

This study identifies NCLX as the primary mitochondrial Ca2+ extruder in hepatocytes, linking hormone-mediated mitochondrial Ca2+ oscillations to gluconeogenesis.

The paper shows BT2 acts as a mitochondrial uncoupler, reducing ROS and lipogenesis, which may explain its therapeutic benefits in metabolic diseases.

This study shows CNTF treatment in degenerating mouse retinas enhances glycolysis and anabolism, improving neuronal viability through metabolic changes.