COASY

Last update 08 May 2025

Basic Info

Synonyms

Bifunctional coenzyme A synthase, CoA synthase, COASY

+ [11]

Introduction

Bifunctional enzyme that catalyzes the fourth and fifth sequential steps of CoA biosynthetic pathway. The fourth reaction is catalyzed by the phosphopantetheine adenylyltransferase, coded by the coaD domain; the fifth reaction is catalyzed by the dephospho-CoA kinase, coded by the coaE domain. May act as a point of CoA biosynthesis regulation.

100 Clinical Results associated with COASY

100 Translational Medicine associated with COASY

0 Patents (Medical) associated with COASY

320

Literatures (Medical) associated with COASY

01 Mar 2025·Clinics and Research in Hepatology and Gastroenterology

Mitochondrial dysfunction in drug-induced hepatic steatosis: Recent findings and current concept

Review

Author: Fromenty, Bernard ; Borgne-Sanchez, Annie

Mitochondrial activity is necessary for the maintenance of many liver functions. In particular, mitochondrial fatty acid oxidation (FAO) is required for energy production and lipid homeostasis. This key metabolic pathway is finely tuned by the mitochondrial respiratory chain (MRC) activity and different transcription factors such as peroxisome proliferator-activated receptor α (PPARα). Many drugs have been shown to cause mitochondrial dysfunction, which can lead to acute and chronic liver lesions. While severe inhibition of mitochondrial FAO would eventually cause microvesicular steatosis, hypoglycemia, and liver failure, moderate impairment of this metabolic pathway can induce macrovacuolar steatosis, which can progress in the long term to steatohepatitis and cirrhosis. Drugs can impair mitochondrial FAO through several mechanisms including direct inhibition of FAO enzymes, sequestration of coenzyme A and l-carnitine, impairment of the activity of one or several MRC complexes and reduced PPARα expression. In drug-induced macrovacuolar steatosis, non-mitochondrial mechanisms can also be involved in lipid accumulation including increased de novo lipogenesis and reduced very-low-density lipoprotein secretion. Nonetheless, mitochondrial dysfunction and subsequent oxidative stress appear to be key events in the progression of steatosis to steatohepatitis. Patients suffering from metabolic dysfunction-associated steatotic liver disease (MASLD) and treated with mitochondriotoxic drugs should be closely monitored to reduce the risk of acute liver injury or a faster transition of steatosis to steatohepatitis. Therapies based on the mitochondrial cofactor l-carnitine, the antioxidant N-acetylcysteine, or thyromimetics might be useful to prevent or treat drug-induced mitochondrial dysfunction, steatosis, and steatohepatitis.

01 Mar 2025·HemaSphere

Low‐risk MDS—A spotlight on precision medicine for SF3B1‐mutated patients

Review

Author: Rouault‐Pierre, Kevin ; Burke, Shoshana ; Chowdhury, Onima

AbstractA deep understanding of the biological mechanisms driving the pathogenesis of myelodysplastic neoplasms (MDS) is essential to develop comprehensive therapeutic approaches that will benefit patient's disease management and quality of life. In this review, we focus on MDS harboring mutations in the splicing factor SF3B1. Clones harboring this mutation arise from the most primitive hematopoietic compartment and expand throughout the entire myeloid lineage, exerting distinct effects at various stages of differentiation. Supportive care, particularly managing anemia, remains essential in SF3B1‐mutated MDS. While SF3B1 mutations are frequently linked with ring sideroblasts and iron overload due to impaired erythropoiesis, the current therapeutic landscape fails to adequately address the underlying disease biology, particularly in transfusion‐dependent patients, where further iron overload contributes to increased morbidity and mortality. Novel agents such as Luspatercept and Imetelstat have shown promise, but their availability remains restricted and their long‐term efficacy is to be investigated. Spliceosome modulators have failed to deliver and inhibitors of inflammatory pathways, including TLR and NF‐κB inhibitors, are still under investigation. This scarcity of effective and disease‐modifying therapies highlights the unmet need for new approaches tailored to the molecular and genetic abnormalities in SF3B1‐mutated MDS. Emerging strategies targeting metabolic mis‐splicing (e.g., COASY) with vitamin B5, pyruvate kinase activators, and inhibitors of oncogenic pathways like MYC and BCL‐2 represent potential future avenues for treatment, but their clinical utility remains to be fully explored. The current limitations in treatment underscore the urgency of developing novel, more effective therapies for patients with SF3B1‐mutated MDS.

01 Feb 2025·Journal of Neurochemistry

Genetic Markers of Postmortem Brain Iron

Article

Author: Fazlollahi, Amir ; Ayton, Scott ; Bennett, David A. ; Cornelis, Marilyn C. ; Schneider, Julie A.

ABSTRACTBrain iron (Fe) dyshomeostasis is implicated in neurodegenerative diseases. Genome‐wide association studies (GWAS) have identified plausible loci correlated with peripheral levels of Fe. Systemic organs and the brain share several Fe regulatory proteins but there likely exist different homeostatic pathways. We performed the first GWAS of inductively coupled plasma mass spectrometry measures of postmortem brain Fe from 635 Rush Memory and Aging Project (MAP) participants. Sixteen single nucleotide polymorphisms (SNPs) associated with Fe in at least one of four brain regions were measured (p < 5 × 10−8). Promising SNPs (p < 5 × 10−6) were followed up for replication in published GWAS of blood, spleen, and brain imaging Fe traits and mapped to candidate genes for targeted cortical transcriptomic and epigenetic analysis of postmortem Fe in MAP. Results for SNPs previously associated with other Fe traits were also examined. Ninety‐eight SNPs associated with postmortem brain Fe were at least nominally (p < 0.05) associated with one or more related Fe traits. Most novel loci identified had no direct links to Fe regulatory pathways but rather endoplasmic reticulum‐Golgi trafficking (SORL1, SORCS2, MARCH1, CLTC), heparan sulfate (HS3ST4, HS3ST1), and coenzyme A (SLC5A6, PANK3); supported by nearest gene function and omic analyses. We replicated (p < 0.05) several previously published Fe loci mapping to candidate genes in cellular and systemic Fe regulation. Finally, novel loci (BMAL, COQ5, SLC25A11) and replication of prior loci (PINK1, PPIF, LONP1) lend support to the role of circadian rhythms and mitochondria function in Fe regulation more generally. In summary, we provide support for novel loci linked to pathways that may have greater relevance to brain Fe accumulation; some of which are implicated in neurodegeneration. However, replication of a subset of prior loci for blood Fe suggests that genetic determinants or biological pathways underlying Fe accumulation in the brain are not completely distinct from those of Fe circulating in the periphery.

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COASY

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