Navdeep S. Chandel

ExPert infers causal perturbations from cell states by learning prototypes across 12 contexts, achieving high recall with low compute and validating findings in disease models.

This paper shows that 2-hydroxyglutarate (2HG) alters fatty acid partitioning, reducing lipotoxic stress by shifting fatty acids toward storage and away from oxidation and membrane synthesis.

This paper constructs a spatial metabolomic atlas of exercise in mice, identifies Complex I as a key target for reducing tau pathology, and shows that enhancing its activity mimics exercise's protective effects.

This study shows that GOT1 and GOT2 have opposing roles in rod photoreceptor health, with GOT2 acting as a neuroprotective factor under reductive stress conditions.

The paper maps spatial metabolome coherence across mouse brain regions using MALDI imaging and optimal transport, showing preserved coherence in Alzheimer's model despite metabolic changes and demonstrating intervention effects.

This study shows that mitochondrial ATP production, induced by D-α-hydroxybutyrate, promotes T cell differentiation and function by regulating chromatin accessibility and gene expression.

This study shows that microglial fructose metabolism via GLUT5 is critical for glioblastoma growth, as GLUT5-KO mice live longer with reduced tumor progression.

This study identifies endothelial PHD3 as a regulator of kidney repair after ischemia, showing its role in suppressing inflammation and fibrosis through HIF-dependent mechanisms.

This study shows that IFNγ suppresses lymphatic vessel growth and metastasis by altering metabolism and immune function in melanoma.

This study shows that influenza A infection accelerates the formation of disease-associated microglia in aging mice, with effects observed in white matter regions.

This study shows that circadian disruption impairs metabolic health by causing mitochondrial complex I dysfunction, which affects adipocyte function and metabolic pathways.

This study shows metformin lowers blood glucose by inhibiting intestinal mitochondrial complex I, increasing lactate and GDF15, and promoting glucose uptake.

This study shows that increasing mitochondrial NAD+ regeneration via MitoLbNOX does not rescue dopaminergic neuron dysfunction caused by complex I impairment in Parkinson's disease mice.

This study identifies aspartate transaminases GOT1 and GOT2 as critical for erythropoiesis by linking metabolism to epigenetic regulation, revealing a novel role in blood development.

The paper identifies ETC regulation as a protective mechanism against excitotoxicity in TRPV1+ sensory neurons using CRISPRi screening and functional experiments.

This study shows G1 and G2 APOL1 variants increase macrophage inflammation and lipid accumulation via the polyamine pathway, which can be inhibited by DFMO.

The paper shows that lipid metabolism, specifically through OA, shifts metabolic pathways in breast cells, increasing SAM and 2-HG, which contribute to oncogenic properties and epigenetic changes.

This study shows that the circadian clock in muscle stem cells modulates immune responses and inflammation during muscle regeneration through NAD+ metabolism and CCL2 signaling.

The paper identifies Complex II's role in de novo purine biosynthesis in AML using CRISPR and metabolomic data, showing it as a therapeutic target.

This study identifies tissue-resident skeletal muscle macrophages that support muscle recovery from viral pneumonia in aging mice, with Mertk playing a key role.

This study shows that inactivating PHD enzymes in endothelial cells after ischemic kidney injury promotes maladaptive repair through glycolysis and MCT4, which can be reversed by MCT4 inhibitors.

This study shows that alpha-synuclein pathology disrupts mitochondrial function in dopaminergic and cholinergic neurons, leading to bioenergetic deficits and neuronal dysfunction in Parkinson's disease.

The paper examines alveolar T cell responses in SARS-CoV-2 pneumonia patients, finding that early interferon signaling and targeting of structural proteins correlate with better clinical outcomes.

This study uses a Drosophila model to show that varying levels of NDUFS1 knockdown lead to distinct phenotypic and metabolic outcomes in complex I deficiency.

This study shows that MOF-mediated H4K16ac is essential for mitochondrial and ciliary functions in mammalian skin development, with loss of MOF causing severe developmental defects.

This study shows octopamine reprograms astrocytes to protect neurons from α-synuclein toxicity through metabolic pathways.

The paper identifies a systemic age-dependent transcriptome imbalance driven by transcript length across multiple species and shows its correlation with splicing factors and environmental stressors.

The paper shows that yeast NDI1 restores metabolite levels, ER-mitochondria contacts, and rescues behavioral and lifespan defects in Drosophila with neuronal complex I deficiency.

This study shows that inhibiting prolyl hydroxylases with DMOG impairs angiogenic competence of human vascular endothelial cells through metabolic reprogramming.

This study shows that mitochondrial acetyl-CoA reversibly modulates histone acetylation and gene expression in models of mtDNA depletion.