T. E. Ryan

A 6-minute Limb Function Assessment for Therapeutic Testing in Experimental Peripheral Artery Disease Models

This paper develops a 6-minute limb function test for preclinical hindlimb ischemia models to assess muscular performance and hemodynamics, showing it detects therapeutic differences better than traditional measures.

Activation of the Aryl Hydrocarbon Receptor in Endothelial Cells Impairs Ischemic Angiogenesis in Chronic Kidney Disease

This study shows that deleting the AHR in endothelial cells improves ischemic angiogenesis in male CKD mice but not females, revealing sex-dependent differences in AHR activation and angiogenic signaling.

Chronic activation of the aryl hydrocarbon receptor in muscle exacerbates ischemic pathology in chronic kidney disease

This study shows chronic AHR activation in muscle worsens ischemic damage in CKD and PAD by impairing muscle function and mitochondrial health.

IGF-1 therapy improves muscle size and function in experimental peripheral arterial disease

This study shows that IGF-1 therapy increases muscle size and strength in a rodent PAD model, with greater effects in female mice.

Skeletal muscle Nox4 knockout prevents and Nox2 knockout blunts loss of maximal diaphragm force in mice with heart failure with reduced ejection fraction

This study shows that Nox4 knockout prevents diaphragm force loss in HFrEF mice, while Nox2 knockout provides partial protection and improves survival after myocardial infarction.

Reversible thiol oxidation increases mitochondrial electron transport complex enzyme activity but not respiration in cardiomyocytes from patients with end-stage heart failure

Chronic Aryl Hydrocarbon Receptor Activity Phenocopies Smoking-induced Skeletal Muscle Impairment

This study shows chronic AHR activation, like from smoking, causes muscle atrophy, mitochondrial issues, and neuromuscular junction damage in mice and humans.

Mitochondrial PE potentiates respiratory enzymes to amplify skeletal muscle aerobic capacity

The paper shows that mitochondrial phospholipids, specifically phosphatidylethanolamine (PE), regulate respiratory capacity in skeletal muscle, with PE deficiency causing respiratory failure and oxidative stress.