Publications by authors named "Naqi Mohammad"
The Aconitate Decarboxylase 1/Itaconate Pathway Modulates Immune Dysregulation and Associates with Cardiovascular Disease Markers and Disease Activity in Systemic Lupus Erythematosus.
J Immunol
August 2024
Article Synopsis
- The enzyme ACOD1 is key in producing itaconate in immune cells, which may help regulate immune responses in lupus.
- In a mouse model of lupus, ACOD1 knockout led to worsened disease symptoms, including increased inflammation and kidney damage compared to normal mice.
- Itaconate levels were found to be lower in lupus patients than in healthy individuals, suggesting its potential use as a therapeutic target for autoimmune diseases.
Article Synopsis
- - Systemic lupus erythematosus (SLE) heightens cardiovascular disease (CVD) risk in patients, and traditional risk factors alone do not account for this increased risk, prompting a need for identifying specific blood immunologic signatures that may help pinpoint at-risk subgroups.
- - A study involving 77 SLE patients and 27 healthy controls assessed cardiovascular metrics like arterial stiffness and coronary plaque through advanced imaging techniques, along with blood analysis via RNA sequencing and inflammatory protein quantification.
- - Results showed higher CAVI, TBR, and noncalcified coronary plaque in SLE patients compared to controls, with specific immune-related genes and serum proteins identified as correlated with increased cardiovascular risk, indicating disrupted immune and metabolic pathways
Objective: The Krebs cycle enzyme Aconitate Decarboxylase 1 (ACOD1) mediates itaconate synthesis in myeloid cells.. Previously, we reported that administration of 4-octyl itaconate abrogated lupus phenotype in mice.
View Article and Find Full Text PDFObjectives: Premature cardiovascular events in systemic lupus erythematosus (SLE) contribute to morbidity and mortality, with no effective preventive strategies described to date. Immune dysregulation and metabolic disturbances appear to play prominent roles in the induction of vascular disease in SLE. The peroxisome proliferator activated receptor-gamma agonist pioglitazone (PGZ suppresses vascular damage and immune dysregulation in murine lupus and improves endothelial dysfunction in other inflammatory diseases.
View Article and Find Full Text PDFIncreased risk of premature cardiovascular disease (CVD) is well recognized in systemic lupus erythematosus (SLE). Aberrant type I-Interferon (IFN)-neutrophil interactions contribute to this enhanced CVD risk. In lupus animal models, the Janus kinase (JAK) inhibitor tofacitinib improves clinical features, immune dysregulation and vascular dysfunction.
View Article and Find Full Text PDFBackground: Systemic lupus erythematosus (SLE) is associated with enhanced risk of atherosclerotic cardiovascular disease not explained by Framingham risk score (FRS). Immune dysregulation associated to a distinct subset of lupus proinflammatory neutrophils (low density granulocytes; LDGs) may play key roles in conferring enhanced CV risk. This study assessed if lupus LDGs are associated with in vivo vascular dysfunction and inflammation and coronary plaque.
View Article and Find Full Text PDFThis cross-sectional study aimed to evaluate the prevalence and predictive factors associated with late HIV diagnoses in Houston, Texas using surveillance data. Study subjects were Houston/Harris County residents, 13 years or older, diagnosed with HIV and reported to the Houston Department of Health and Human Services. Late HIV diagnosis was defined as an AIDS diagnosis within three months of an HIV diagnosis.
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