Results 51 to 60 of about 354 (136)
Inflammation in cardiovascular disease is a dynamic and context‐dependent network rather than a secondary response to injury. Mitochondrial danger signaling links metabolic stress to immune activation through TLR priming, NLRP3 inflammasome amplification, cGAS–STING signaling, and immunometabolic gating, providing a basis for more precise therapeutic ...
Jiaxiang Rong +8 more
wiley +1 more source
Exploration of Novel Urolithin C Derivatives as Non-Competitive Inhibitors of Liver Pyruvate Kinase
The inhibition of liver pyruvate kinase could be beneficial to halt or reverse non-alcoholic fatty liver disease (NAFLD), a progressive accumulation of fat in the liver that can lead eventually to cirrhosis.
Umberto Maria Battisti +12 more
doaj +1 more source
Type 2 Diabetes Mellitus: Molecular Pathogenesis and Therapeutic Interventions
This graphical summary illustrates the multiorgan therapeutic landscape for Type 2 diabetes mellitus (T2D), integrating molecular pathogenesis with modern treatment strategies. It depicts how current interventions, including SGLT2 inhibitors, GLP‐1 receptor agonists, and insulin secretagogues, target key organs—kidney, pancreas, gastrointestinal tract,
Shinuan Fei +9 more
wiley +1 more source
Ammonia Metabolism in the Aging Liver: Emerging Mechanistic Insights
Liver aging may weaken ammonia‐detoxification reserve by disrupting mitochondrial ureagenesis, GS‐mediated scavenging, glutamine metabolism, and metabolic zonation. This emerging framework links impaired nitrogen handling to potential hepatic stress amplification and systemic crosstalk, while highlighting the need for direct validation in physiological
Heng Zhang, Guangyu Liang, Anding Liu
wiley +1 more source
Background Myocardial fibrosis after myocardial infarction (MI) is one of the leading causes of cardiovascular diseases. Cardiac fibroblasts (CFs) are activated and promoted by MI to undergo myofibroblast transformation (CMT).
Pengfei Chen +5 more
doaj +1 more source
Advances in the Core Role and Mechanisms of Mitochondrial Dysfunction in Alzheimer's Disease
In Alzheimer's disease, Aβ and Tau trigger mitochondrial dysfunction, driving a pathological cascade that results in cognitive decline. Gut microbiota dysbiosis exacerbates this via the gut–brain axis, making mitochondria a key therapeutic target. ABSTRACT Introduction Alzheimer's disease (AD) is a complex neurodegenerative disorder whose pathogenesis ...
Tianyi Gu +3 more
wiley +1 more source
The journal retracts the article titled “A Combination Therapy of Urolithin A+EGCG Has Stronger Protective Effects than Single Drug Urolithin A in a Humanized Amyloid Beta Knockin Mice for Late-Onset Alzheimer’s Disease” [...]
Sudhir Kshirsagar +8 more
doaj +1 more source
Background Osteoarthritis (OA) is characterized by inflammation and extracellular matrix (ECM) degradation and is one of the most common chronic degenerative joint diseases that causes pain and disability in adults.
Sheng-long Ding +7 more
doaj +1 more source
Urolithin A, a gut microbial metabolite, binds TNF to suppress proliferation, inflammation, and oxidative stress, offering a promising microbe‐derived therapeutic avenue for pulmonary hypertension. ABSTRACT Pulmonary hypertension (PH) is a complex and multifactorial disease that poses a significant clinical challenge.
Yujie Qu +8 more
wiley +1 more source
Urolithin A (UA) is a gut microbiota‐derived metabolite produced from dietary ellagitannins and ellagic acid, with endogenous formation varying among urolithin metabotypes (UM‐A, UM‐B, and UM‐0). UA regulates an interconnected network centered on mitophagy and mitochondrial quality control, antioxidant defense, inflammatory signaling, autophagy, and ...
Zijiang Yang +3 more
wiley +1 more source

