Results 61 to 70 of about 12,683 (169)

STAT3 and mutp53 Engage a Positive Feedback Loop Involving HSP90 and the Mevalonate Pathway

open access: yesFrontiers in Oncology, 2020
Oncosuppressor TP53 and oncogene STAT3 have been shown to engage an interplay in which they negatively influence each other. Conversely, mutant (mut) p53 may sustain STAT3 phosphorylation by displacing SH2 phosphatase while whether STAT3 could influence ...
Maria Anele Romeo   +11 more
doaj   +1 more source

Mechanisms and Predisposing Conditions for Statin‐Induced New‐Onset Type 2 Diabetes Mellitus: A Paradox Relative to Their Pleiotropic Metabolic Effects

open access: yesEndocrinology, Diabetes &Metabolism, Volume 9, Issue 5, September 2026.
The primary function of statins is to inhibit cholesterol synthesis, which contributes to their antidiabetic effects. However, the majority of the diabetic effects of statins are due to inhibition of isoprenoid synthesis. Atorvastatin, simvastatin and rosuvastatin possess the most pronounced diabetogenic properties. In contrast, lovastatin, fluvastatin,
Ali Nosrati Andevari, Mohsen Koolivand
wiley   +1 more source

Changes in chick liver and brain mevalonate kinase, mevalonate-5-phosphate kinase and mevalonate-5-pyrophosphate decarboxylase during development

open access: yesInternational Journal of Biochemistry, 1984
Phosphorylation and decarboxylation of mevalonate in chick liver and brain was investigated during early post hatching stages of development. In chick liver, both mevalonate kinase and mevalonate-5-phosphate kinase increased their activity from day 5 of age while pyrophosphate decarboxylase activity remained low during the first days after hatching ...
D, Gonzalez-Pacanowska   +3 more
openaire   +5 more sources

Weekly oral alendronate in mevalonate kinase deficiency [PDF]

open access: yesOrphanet Journal of Rare Diseases, 2013
Mevalonate kinase deficiency (MKD) is caused by mutations in the MVK gene, encoding the second enzyme of mevalonate pathway, which results in subsequent shortage of downstream compounds, and starts in childhood with febrile attacks, skin, joint, and gastrointestinal symptoms, sometimes induced by vaccinations.For a history of early-onset corticosteroid-
Cantarini L.   +7 more
openaire   +6 more sources

Oxysterols in Cancer: From Biosynthesis and Pathophysiology to Targeted Therapeutics

open access: yesMedComm – Oncology, Volume 5, Issue 3, September 2026.
Mechanisms by which oxysterol targeting may enhance immunotherapy efficacy. This figure illustrates potential metabolic interventions that may improve antitumor immunity by modulating oxysterol related pathways. CH25H modulation may reduce 25‐HC accumulation, promote the conversion of cold tumors into hot tumors, and increase T cell infiltration and PD‐
Haili Shang, Yongsheng Li
wiley   +1 more source

Overcoming Radiation Resistance: Ferroptosis Induction to Sensitize Solid Tumors to Radiation Therapy

open access: yesCancer Medicine, Volume 15, Issue 8, August 2026.
ABSTRACT Radiation therapy (RT) is a mainstay of treatment for a myriad of cancers, often utilized for tumors that are unable to be resected, as well as an adjunct to surgery and chemotherapy. Unfortunately, many cancers are resistant to RT‐induced damage and subsequent cell death.
Joseph Carmicheal   +4 more
wiley   +1 more source

Identification of two novel MVD mutations and one novel FDPS mutation in Chinese patients with porokeratosis

open access: yesFrontiers in Medicine
BackgroundPorokeratosis (PK) is an autosomal dominant inherited disorder characterized by abnormal epidermal keratinization, primarily resulting from mutations in four genes associated with the mevalonate pathway: mevalonate decarboxylase (MVD ...
Yang He   +7 more
doaj   +1 more source

Discontinuing Long‐Term Denosumab in Treating Fragile Bone: Why, for Whom, and How?

open access: yesClinical Pharmacology &Therapeutics, Volume 120, Issue 2, Page 334-344, August 2026.
Discontinuation of denosumab (Dmab) may be necessary due to adverse events or an unfavorable long‐term risk–benefit profile. However, accumulating evidence demonstrates pronounced rebound phenomena after withdrawal, most notably a marked increase in multiple vertebral fractures, and, in some reports, elevated mortality.
Ko‐Hsiu Lu   +5 more
wiley   +1 more source

Uncovering Coenzyme Q10‐Related Genetic Determinants of Statin‐Associated Muscle Symptoms: Evidence from the UK Biobank and the All of Us Research Program

open access: yesClinical Pharmacology &Therapeutics, Volume 120, Issue 2, Page 475-483, August 2026.
Statin‐associated muscle symptoms (SAMS) are frequent adverse effects of statin therapy and have been hypothesized to result from impaired coenzyme Q10 (CoQ10) biosynthesis. Although genetic determinants of CoQ10 levels have been reported, genome‐wide association studies (GWASs) conducted specifically in statin users are lacking. Moreover, direct CoQ10
Da Hoon Lee   +6 more
wiley   +1 more source

Myocardial Lipid Metabolism Imbalance: The Pathological Core and Novel Diagnostic‐Therapeutic Directions of Cardiovascular Diseases

open access: yesJournal of Biochemical and Molecular Toxicology, Volume 40, Issue 8, August 2026.
In cardiac cells, Plin5/AMPK regulate lipid homeostasis; excess CD36‐mediated uptake drives lipotoxicity, mitochondrial dysfunction, and CVDs (e.g., heart failure). Biomarkers (ApoB/ApoA‐1) and therapies (SGLT2 inhibitors) target this cascade. ABSTRACT Cardiac lipid metabolism is fundamental to myocardial energy homeostasis, with fatty acid oxidation ...
Peiyun Xie   +3 more
wiley   +1 more source

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