Garrett M. Fogo

ORCID: 0000-0001-5292-3702
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About
Contact & Profiles
Research Areas
  • Mitochondrial Function and Pathology
  • ATP Synthase and ATPases Research
  • Circadian rhythm and melatonin
  • Traumatic Brain Injury and Neurovascular Disturbances
  • Anesthesia and Neurotoxicity Research
  • Cardiac Arrest and Resuscitation
  • Schizophrenia research and treatment
  • Adipose Tissue and Metabolism
  • Spaceflight effects on biology
  • Mechanical Circulatory Support Devices
  • Spectroscopy Techniques in Biomedical and Chemical Research
  • Immune Cell Function and Interaction
  • Metabolomics and Mass Spectrometry Studies
  • Ubiquitin and proteasome pathways
  • Tryptophan and brain disorders
  • Immunotherapy and Immune Responses
  • Phagocytosis and Immune Regulation
  • Iron Metabolism and Disorders
  • Photoreceptor and optogenetics research
  • Metabolism and Genetic Disorders
  • Bat Biology and Ecology Studies
  • Retinal Development and Disorders
  • Heme Oxygenase-1 and Carbon Monoxide
  • T-cell and B-cell Immunology
  • Autophagy in Disease and Therapy

Brigham and Women's Hospital
2025

Harvard University
2025

University of Michigan–Ann Arbor
2019-2024

Hope College
2018-2019

Mitochondrial form and function are regulated by the opposing forces of mitochondrial dynamics: fission fusion. dynamics highly active consequential during neuronal ischemia/reperfusion (I/R) injury. fusion is executed at inner membrane Opa1. The balance long (L-Opa1) proteolytically cleaved short (S-Opa1) isoforms critical for efficient Oma1 predominant stress-responsive protease Opa1 processing. In cell models, we assessed regulation stress. an immortalized mouse hippocampal neuron line...

10.1096/fj.202400313r article EN cc-by-nc-nd The FASEB Journal 2024-09-23

Mitochondrial damage and dysfunction are hallmarks of neuronal injury during cerebral ischemia-reperfusion (I/R). Critical mitochondrial functions including energy production cell signaling perturbed I/R, often exacerbating contributing to secondary injury. The integrity the proteome is essential for efficient function. proteostasis mediated by cooperative forces mitophagy intramitochondrial proteolysis. aim this study was elucidate patterns protein dynamics their key regulators an in vitro...

10.1080/15548627.2025.2472586 article EN cc-by-nc-nd Autophagy 2025-02-27

Abstract The mitochondrial network continually undergoes events of fission and fusion. Under physiologic conditions, the is in equilibrium characterized by presence both elongated punctate mitochondria. However, this balanced, homeostatic profile can change morphologic distribution response to various stressors. Therefore, it imperative develop a method that robustly measures morphology with high accuracy. Here, we developed semi-automated image analysis pipeline for quantitation vitro vivo...

10.1038/s41598-021-84528-8 article EN cc-by Scientific Reports 2021-03-04

Abstract Mitochondrial dynamics and mitophagy are constitutive complex systems that ensure a healthy mitochondrial network through the segregation subsequent degradation of damaged mitochondria. Disruption these can lead to dysfunction has been established as central mechanism ischemia/reperfusion (I/R) injury. Emerging evidence suggests integrated systems; however, role this relationship in context I/R injury remains unclear. To investigate concept, we utilized primary cortical neurons...

10.1038/s41419-021-03752-2 article EN cc-by Cell Death and Disease 2021-05-12

In response to an immune challenge, naive T cells undergo a transition from quiescent activated state acquiring the effector function. Concurrently, these reprogram cellular metabolism, which is regulated by iron. We and others have shown that iron homeostasis controls proliferation mitochondrial function, but underlying mechanisms are poorly understood. Given derived heme makes up large portion of pool, we investigated in using mice with cell-specific deletion exporter, FLVCR1 [referred as...

10.1073/pnas.2318420121 article EN Proceedings of the National Academy of Sciences 2024-04-15

Abstract Background Brain injury is a leading cause of morbidity and mortality in patients resuscitated from cardiac arrest. Mitochondrial dysfunction contributes to brain following arrest; therefore, therapies that limit mitochondrial have the potential improve neurological outcomes. Generation reactive oxygen species (ROS) during ischemia–reperfusion critical component dependent on hyperactivation mitochondria resuscitation. Our previous studies provided evidence modulating function with...

10.1186/s13054-023-04745-7 article EN cc-by Critical Care 2023-12-14

Environmental conditions, such as the light-dark cycle and temperature, affect display of circadian rhythmicity locomotor activity patterns in mammals. Here, we tested hypothesis that manipulating these environmental conditions would wheel-running a diurnal rodent, Nile grass rat (Arvicanthis niloticus). Grass rats are field, however, subset switch from day-active pattern to night-active after introduction running wheel. The mechanism this chronotype remains largely unknown. In present...

10.1037/com0000154 article EN Deleted Journal 2018-11-05

Extracorporeal cardiopulmonary resuscitation (ECPR) is emerging as a feasible and effective rescue strategy for prolonged cardiac arrest (CA). However, total body ischemia reperfusion can cause microvascular occlusion that prevents organ recovery of function. One hypothesized mechanism "no-reflow" leukocyte adhesion formation neutrophil extracellular traps. In this study we tested the hypothesis filter (LF) or modulation device (L-MOD) could reduce NETosis improve heart brain function in...

10.1038/s41598-024-63522-w article EN cc-by Scientific Reports 2024-06-07
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