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Article ; Online: Appreciation Note for Simon C. Roe, Deputy Editor-in-Chief.

Johnson, Kenneth A

Veterinary and comparative orthopaedics and traumatology : V.C.O.T

2022 Volume 35, Issue 6, Page(s) vi

Language	English
Publishing date	2022-11-17
Publishing country	Germany
Document type	Journal Article
ZDB-ID	286750-3
ISSN	2567-6911 ; 0932-0814
ISSN (online)	2567-6911
ISSN	0932-0814
DOI	10.1055/s-0042-1758568
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Article ; Online: The immune system as a driver of mitochondrial disease pathogenesis: a review of evidence.

Hanaford, Allison / Johnson, Simon C

Orphanet journal of rare diseases

2022 Volume 17, Issue 1, Page(s) 335

Abstract: Background: Genetic mitochondrial diseases represent a significant challenge to human health. These diseases are extraordinarily heterogeneous in clinical presentation and genetic origin, and often involve multi-system disease with severe progressive ... ...

Abstract	Background: Genetic mitochondrial diseases represent a significant challenge to human health. These diseases are extraordinarily heterogeneous in clinical presentation and genetic origin, and often involve multi-system disease with severe progressive symptoms. Mitochondrial diseases represent the most common cause of inherited metabolic disorders and one of the most common causes of inherited neurologic diseases, yet no proven therapeutic strategies yet exist. The basic cell and molecular mechanisms underlying the pathogenesis of mitochondrial diseases have not been resolved, hampering efforts to develop therapeutic agents. Main body: In recent pre-clinical work, we have shown that pharmacologic agents targeting the immune system can prevent disease in the Ndufs4(KO) model of Leigh syndrome, indicating that the immune system plays a causal role in the pathogenesis of at least this form of mitochondrial disease. Intriguingly, a number of case reports have indicated that immune-targeting therapeutics may be beneficial in the setting of genetic mitochondrial disease. Here, we summarize clinical and pre-clinical evidence suggesting a key role for the immune system in mediating the pathogenesis of at least some forms of genetic mitochondrial disease. Conclusions: Significant clinical and pre-clinical evidence indicates a key role for the immune system as a significant in the pathogenesis of at least some forms of genetic mitochondrial disease.
MeSH term(s)	Humans ; Immune System/metabolism ; Leigh Disease/genetics ; Leigh Disease/metabolism ; Mitochondria/metabolism ; Mitochondrial Diseases/genetics ; Nervous System Diseases/metabolism
Language	English
Publishing date	2022-09-02
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2225857-7
ISSN	1750-1172 ; 1750-1172
ISSN (online)	1750-1172
ISSN	1750-1172
DOI	10.1186/s13023-022-02495-3
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Article ; Online: The immune system as a driver of mitochondrial disease pathogenesis

Allison Hanaford / Simon C. Johnson

Orphanet Journal of Rare Diseases, Vol 17, Iss 1, Pp 1-

a review of evidence

2022 Volume 12

Abstract: Abstract Background Genetic mitochondrial diseases represent a significant challenge to human health. These diseases are extraordinarily heterogeneous in clinical presentation and genetic origin, and often involve multi-system disease with severe ... ...

Abstract	Abstract Background Genetic mitochondrial diseases represent a significant challenge to human health. These diseases are extraordinarily heterogeneous in clinical presentation and genetic origin, and often involve multi-system disease with severe progressive symptoms. Mitochondrial diseases represent the most common cause of inherited metabolic disorders and one of the most common causes of inherited neurologic diseases, yet no proven therapeutic strategies yet exist. The basic cell and molecular mechanisms underlying the pathogenesis of mitochondrial diseases have not been resolved, hampering efforts to develop therapeutic agents. Main body In recent pre-clinical work, we have shown that pharmacologic agents targeting the immune system can prevent disease in the Ndufs4(KO) model of Leigh syndrome, indicating that the immune system plays a causal role in the pathogenesis of at least this form of mitochondrial disease. Intriguingly, a number of case reports have indicated that immune-targeting therapeutics may be beneficial in the setting of genetic mitochondrial disease. Here, we summarize clinical and pre-clinical evidence suggesting a key role for the immune system in mediating the pathogenesis of at least some forms of genetic mitochondrial disease. Conclusions Significant clinical and pre-clinical evidence indicates a key role for the immune system as a significant in the pathogenesis of at least some forms of genetic mitochondrial disease.
Keywords	Mitochondrial disease ; Leigh syndrome ; MELAS ; Immunity ; Genetic disease ; Medicine ; R
Language	English
Publishing date	2022-09-01T00:00:00Z
Publisher	BMC
Document type	Article ; Online
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Article: Nutrient Sensing, Signaling and Ageing: The Role of IGF-1 and mTOR in Ageing and Age-Related Disease.

Johnson, Simon C

Sub-cellular biochemistry

2019 Volume 90, Page(s) 49–97

Abstract: Nutrient signaling through insulin/IGF-1 was the first pathway demonstrated to regulate ageing and age-related disease in model organisms. Pharmacological or dietary interventions targeting nutrient signaling pathways have been shown to robustly ... ...

Abstract	Nutrient signaling through insulin/IGF-1 was the first pathway demonstrated to regulate ageing and age-related disease in model organisms. Pharmacological or dietary interventions targeting nutrient signaling pathways have been shown to robustly attenuate ageing in many organisms. Caloric restriction, the most widely studied longevity promoting intervention, works through multiple nutrient signaling pathways, while inhibition of mTOR through treatment with rapamycin reproducibly delays ageing and disease through specific inhibition of the mTOR complexes. Although the benefits of reduced insulin/IGF-1 in lifespan and health are well documented in model organisms, defining the precise role of the IGF-1 in human ageing and age-related disease has proven more difficult. Association studies provide some insight but also reveal paradoxes. Low serum IGF-1 predicts longevity, but IGF-1 decreases with age and IGF-1 therapy benefits some of age-related pathologies. Circulating IGF-1 has been associated both positively and negatively with risk of age-related diseases in humans, and in some cases both activation and inhibition of IGF-1 signaling have provided benefit in animal models of the same diseases. Interventions designed modulate the nutrient sensing signaling pathways positively or negatively are already available for clinical use, highlighting the need for a clear understanding of the role of nutrient signaling in ageing and age-related disease. This chapter examines data from model organisms and human genetic association studies, with a special emphasis on IGF-1 and mTOR, and discusses potential models for resolving the paradoxes surrounding IGF-1 data.
MeSH term(s)	Aging/metabolism ; Aging/pathology ; Animals ; Humans ; Insulin-Like Growth Factor I/metabolism ; Longevity ; Nutrients/metabolism ; Signal Transduction ; TOR Serine-Threonine Kinases/metabolism
Chemical Substances	Nutrients ; Insulin-Like Growth Factor I (67763-96-6) ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.1.1)
Language	English
Publishing date	2019-02-18
Publishing country	United States
Document type	Journal Article ; Review
ISSN	0306-0225 ; 0096-8757
ISSN	0306-0225 ; 0096-8757
DOI	10.1007/978-981-13-2835-0_3
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Article: A chylothorax in a young woman: The difficulties of medical management.

Barton, Eleanor C / Johnson, Simon / Collin, Neil / Bhatt, Nidhi / Maskell, Nick A

Respirology case reports

2024 Volume 12, Issue 2, Page(s) e01303

Abstract: Lymphangioleiomyomatosis is a rare pulmonary disease affecting women of childbearing age. Whilst chylothorax is a well-recognized complication of the condition, management strategies aren't well-defined, have low success rates and are often only ... ...

Abstract	Lymphangioleiomyomatosis is a rare pulmonary disease affecting women of childbearing age. Whilst chylothorax is a well-recognized complication of the condition, management strategies aren't well-defined, have low success rates and are often only available at tertiary or specialist centres. We describe a case of a young woman referred to pleural clinic with a chylous effusion found to be secondary to lymphangioleiomyomatosis. Initial medical management was unsuccessful and recurrent drainages caused significant complications. Remission was ultimately achieved with a combination of mTOR inhibitors and interventional radiology techniques.
Language	English
Publishing date	2024-02-15
Publishing country	United States
Document type	Case Reports
ZDB-ID	2750180-2
ISSN	2051-3380
ISSN	2051-3380
DOI	10.1002/rcr2.1303
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Article ; Online: The effect of tenotomy, neurotomy, and dual injury on mouse rotator cuff muscles: Consequences for the mouse as a preclinical model.

Gibbons, Michael C / Silldorff, Morgan / Okuno, Hiroshi / Esparza, Mary C / Migdal, Christopher / Johnson, Seth / Schenk, Simon / Ward, Samuel R

Journal of orthopaedic research : official publication of the Orthopaedic Research Society

2024 Volume 42, Issue 6, Page(s) 1170–1179

Abstract: A common animal model of muscle pathology following rotator cuff tear (RCT) is a tenotomy of the supraspinatus and infraspinatus, often combined with neurotomy of the suprascapular nerve, which induces a more robust atrophy response than tenotomy alone. ... ...

Abstract	A common animal model of muscle pathology following rotator cuff tear (RCT) is a tenotomy of the supraspinatus and infraspinatus, often combined with neurotomy of the suprascapular nerve, which induces a more robust atrophy response than tenotomy alone. However, the utility of this model depends on its similarity to human muscle pathology post-RCT, both in terms of the disease phenotype and mechanisms of muscle atrophy and fatty infiltration. Given the clinical prevalence of nerve injury is low and the muscular response to denervation is distinct from mechanical unloading in other models, an understanding of the biological influence of the nerve injury is critical for interpreting data from this RCT model. We evaluated the individual and combined effect of tenotomy and neurotomy across multiple biological scales, in a robust time-series in the mouse supraspinatus. Muscle composition, histological, and gene expression data related to muscle atrophy, degeneration-regeneration, fatty infiltration, and fibrosis were evaluated. Broadly, we found tenotomy alone caused small, transient changes in these pathological features, which resolved over the course of the study, while neurotomy alone caused a significant fatty atrophy phenotype. The dual injury group had a similar fatty atrophy phenotype to the neurotomy group, though the addition of tenotomy did marginally enhance the fat and connective tissue. Overall, these results suggest the most clinically relevant injury model, tenotomy alone, does not produce a clinically relevant phenotype. The dual injury model partially recapitulates the human condition, but it does so through a nerve injury, which is not well justified clinically.
MeSH term(s)	Animals ; Tenotomy ; Rotator Cuff Injuries/surgery ; Rotator Cuff Injuries/pathology ; Muscular Atrophy/etiology ; Disease Models, Animal ; Mice, Inbred C57BL ; Rotator Cuff/surgery ; Rotator Cuff/pathology ; Rotator Cuff/innervation ; Male ; Mice
Language	English
Publishing date	2024-01-21
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	605542-4
ISSN	1554-527X ; 0736-0266
ISSN (online)	1554-527X
ISSN	0736-0266
DOI	10.1002/jor.25786
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Article ; Online: Predicting suicide death after emergency department visits with mental health or self-harm diagnoses.

Simon, Gregory E / Johnson, Eric / Shortreed, Susan M / Ziebell, Rebecca A / Rossom, Rebecca C / Ahmedani, Brian K / Coleman, Karen J / Beck, Arne / Lynch, Frances L / Daida, Yihe G

General hospital psychiatry

2024 Volume 87, Page(s) 13–19

Abstract: Objective: Use health records data to predict suicide death following emergency department visits.: Methods: Electronic health records and insurance claims from seven health systems were used to: identify emergency department visits with mental ... ...

Abstract	Objective: Use health records data to predict suicide death following emergency department visits. Methods: Electronic health records and insurance claims from seven health systems were used to: identify emergency department visits with mental health or self-harm diagnoses by members aged 11 or older; extract approximately 2500 potential predictors including demographic, historical, and baseline clinical characteristics; and ascertain subsequent deaths by self-harm. Logistic regression with lasso and random forest models predicted self-harm death over 90 days after each visit. Results: Records identified 2,069,170 eligible visits, 899 followed by suicide death within 90 days. The best-fitting logistic regression with lasso model yielded an area under the receiver operating curve of 0.823 (95% CI 0.810-0.836). Visits above the 95th percentile of predicted risk included 34.8% (95% CI 31.1-38.7) of subsequent suicide deaths and had a 0.303% (95% CI 0.261-0.346) suicide death rate over the following 90 days. Model performance was similar across subgroups defined by age, sex, race, and ethnicity. Conclusions: Machine learning models using coded data from health records have moderate performance in predicting suicide death following emergency department visits for mental health or self-harm diagnosis and could be used to identify patients needing more systematic follow-up.
MeSH term(s)	Humans ; Mental Health ; Emergency Room Visits ; Suicide/psychology ; Self-Injurious Behavior/epidemiology ; Emergency Service, Hospital
Language	English
Publishing date	2024-01-22
Publishing country	United States
Document type	Journal Article
ZDB-ID	392299-6
ISSN	1873-7714 ; 0163-8343
ISSN (online)	1873-7714
ISSN	0163-8343
DOI	10.1016/j.genhosppsych.2024.01.009
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Zs.A 1584: Show issues

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Article ; Online: Glutamine metabolism in diseases associated with mitochondrial dysfunction.

Bornstein, Rebecca / Mulholland, Michael T / Sedensky, Margaret / Morgan, Phil / Johnson, Simon C

Molecular and cellular neurosciences

2023 Volume 126, Page(s) 103887

Abstract: Mitochondrial dysfunction can arise from genetic defects or environmental exposures and impact a wide range of biological processes. Among these are metabolic pathways involved in glutamine catabolism, anabolism, and glutamine-glutamate cycling. In ... ...

Abstract	Mitochondrial dysfunction can arise from genetic defects or environmental exposures and impact a wide range of biological processes. Among these are metabolic pathways involved in glutamine catabolism, anabolism, and glutamine-glutamate cycling. In recent years, altered glutamine metabolism has been found to play important roles in the pathologic consequences of mitochondrial dysfunction. Glutamine is a pleiotropic molecule, not only providing an alternate carbon source to glucose in certain conditions, but also playing unique roles in cellular communication in neurons and astrocytes. Glutamine consumption and catabolic flux can be significantly altered in settings of genetic mitochondrial defects or exposure to mitochondrial toxins, and alterations to glutamine metabolism appears to play a particularly significant role in neurodegenerative diseases. These include primary mitochondrial diseases like Leigh syndrome (subacute necrotizing encephalopathy) and MELAS (mitochondrial myopathy with encephalopathy, lactic acidosis, and stroke-like episodes), as well as complex age-related neurodegenerative disorders such as Alzheimer's and Parkinson's diseases. Pharmacologic interventions targeting glutamine metabolizing and catabolizing pathways appear to provide some benefits in cell and animal models of these diseases, indicating glutamine metabolism may be a clinically relevant target. In this review, we discuss glutamine metabolism, mitochondrial disease, the impact of mitochondrial dysfunction on glutamine metabolic processes, glutamine in neurodegeneration, and candidate targets for therapeutic intervention.
MeSH term(s)	Animals ; Glutamine/metabolism ; Glutamine/therapeutic use ; MELAS Syndrome/drug therapy ; MELAS Syndrome/genetics ; Mitochondria/metabolism ; Neurodegenerative Diseases/metabolism ; Mitochondrial Diseases/metabolism
Chemical Substances	Glutamine (0RH81L854J)
Language	English
Publishing date	2023-08-15
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural
ZDB-ID	1046640-x
ISSN	1095-9327 ; 1044-7431
ISSN (online)	1095-9327
ISSN	1044-7431
DOI	10.1016/j.mcn.2023.103887
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Article ; Online: Anthracyclines induce cardiotoxicity through a shared gene expression response signature.

Matthews, E Renee / Johnson, Omar D / Horn, Kandace J / Gutiérrez, José A / Powell, Simon R / Ward, Michelle C

PLoS genetics

2024 Volume 20, Issue 2, Page(s) e1011164

Abstract: TOP2 inhibitors (TOP2i) are effective drugs for breast cancer treatment. However, they can cause cardiotoxicity in some women. The most widely used TOP2i include anthracyclines (AC) Doxorubicin (DOX), Daunorubicin (DNR), Epirubicin (EPI), and the ... ...

Abstract	TOP2 inhibitors (TOP2i) are effective drugs for breast cancer treatment. However, they can cause cardiotoxicity in some women. The most widely used TOP2i include anthracyclines (AC) Doxorubicin (DOX), Daunorubicin (DNR), Epirubicin (EPI), and the anthraquinone Mitoxantrone (MTX). It is unclear whether women would experience the same adverse effects from all drugs in this class, or if specific drugs would be preferable for certain individuals based on their cardiotoxicity risk profile. To investigate this, we studied the effects of treatment of DOX, DNR, EPI, MTX, and an unrelated monoclonal antibody Trastuzumab (TRZ) on iPSC-derived cardiomyocytes (iPSC-CMs) from six healthy females. All TOP2i induce cell death at concentrations observed in cancer patient serum, while TRZ does not. A sub-lethal dose of all TOP2i induces limited cellular stress but affects calcium handling, a function critical for cardiomyocyte contraction. TOP2i induce thousands of gene expression changes over time, giving rise to four distinct gene expression response signatures, denoted as TOP2i early-acute, early-sustained, and late response genes, and non-response genes. There is no drug- or AC-specific signature. TOP2i early response genes are enriched in chromatin regulators, which mediate AC sensitivity across breast cancer patients. However, there is increased transcriptional variability between individuals following AC treatments. To investigate potential genetic effects on response variability, we first identified a reported set of expression quantitative trait loci (eQTLs) uncovered following DOX treatment in iPSC-CMs. Indeed, DOX response eQTLs are enriched in genes that respond to all TOP2i. Next, we identified 38 genes in loci associated with AC toxicity by GWAS or TWAS. Two thirds of the genes that respond to at least one TOP2i, respond to all ACs with the same direction of effect. Our data demonstrate that TOP2i induce thousands of shared gene expression changes in cardiomyocytes, including genes near SNPs associated with inter-individual variation in response to DOX treatment and AC-induced cardiotoxicity.
MeSH term(s)	Humans ; Female ; Anthracyclines/adverse effects ; Anthracyclines/metabolism ; Cardiotoxicity/genetics ; Cardiotoxicity/metabolism ; Antibiotics, Antineoplastic/adverse effects ; Antibiotics, Antineoplastic/metabolism ; Topoisomerase II Inhibitors/metabolism ; Topoisomerase II Inhibitors/pharmacology ; Doxorubicin/adverse effects ; Doxorubicin/metabolism ; Mitoxantrone/adverse effects ; Mitoxantrone/metabolism ; Myocytes, Cardiac/metabolism ; Daunorubicin/metabolism ; Daunorubicin/pharmacology ; Epirubicin/metabolism ; Epirubicin/pharmacology ; DNA Topoisomerases, Type II/genetics ; Gene Expression
Chemical Substances	Anthracyclines ; Antibiotics, Antineoplastic ; Topoisomerase II Inhibitors ; Doxorubicin (80168379AG) ; Mitoxantrone (BZ114NVM5P) ; Daunorubicin (ZS7284E0ZP) ; Epirubicin (3Z8479ZZ5X) ; DNA Topoisomerases, Type II (EC 5.99.1.3)
Language	English
Publishing date	2024-02-28
Publishing country	United States
Document type	Journal Article
ZDB-ID	2186725-2
ISSN	1553-7404 ; 1553-7390
ISSN (online)	1553-7404
ISSN	1553-7390
DOI	10.1371/journal.pgen.1011164
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Article ; Online: From the Blood-Brain Barrier to Childhood Development: A Case of Acute-Onset Psychosis and Cognitive Impairment Attributed to Systemic Lupus Erythematosus in an Adolescent Female.

Johnson, Matthew C / Sathappan, Aakash / Hanly, John G / Ross, Gail S / Hauptman, Aaron J / Stone, William S / Simon, Kevin M

Harvard review of psychiatry

2022 Volume 30, Issue 1, Page(s) 71–82

Abstract: Learning objectives: After participating in this CME activity, the clinician will be better able to:• Interpret classifications of neuropsychiatric systemic lupus erythematosus (NPSLE).• Identify determining factors of neuropsychiatric events.• Analyze ... ...

Abstract	Learning objectives: After participating in this CME activity, the clinician will be better able to:• Interpret classifications of neuropsychiatric systemic lupus erythematosus (NPSLE).• Identify determining factors of neuropsychiatric events.• Analyze current evidence regarding disease pathways for NPSLE.
MeSH term(s)	Adolescent ; Blood-Brain Barrier ; Child ; Cognitive Dysfunction/etiology ; Female ; Humans ; Lupus Erythematosus, Systemic/complications ; Lupus Vasculitis, Central Nervous System ; Psychotic Disorders/etiology
Language	English
Publishing date	2022-01-13
Publishing country	United States
Document type	Case Reports ; Journal Article
ZDB-ID	1174775-4
ISSN	1465-7309 ; 1067-3229
ISSN (online)	1465-7309
ISSN	1067-3229
DOI	10.1097/HRP.0000000000000315
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