Results 71 to 80 of about 2,315 (156)
Tafazzin (TAZ) protein has been upregulated in various types of human cancers, although the basis for elevation is uncertain, it has been made definite that the effect of mutation in the hippo pathway, particularly when it is switched off, considerably ...
Madhumala Gopinath +11 more
doaj
In this article, the formation of prokaryotic and eukaryotic cardiolipin is reviewed in light of its biological function. I begin with a detailed account of the structure of cardiolipin, its stereochemistry, and the resulting physical properties, and I ...
Michael Schlame
doaj +1 more source
Barth syndrome (BTHS) is a rare genetic disorder due to mutations in the TAFAZZIN gene, leading to impaired maturation of cardiolipin and thereby adversely affecting mitochondrial function and energy metabolism, often resulting in cardiomyopathy.
Amanda A. Greenwell +28 more
doaj +1 more source
This review highlights mitochondrial dysfunction as a central driver of pancreatic β cell failure in diabetes, caused by disrupted mitochondrial quality control (MQC), oxidative stress, and impaired organelle communication. Emerging therapies, such as DRAK2 inhibitors and metabolic reprogramming agents, show promise in restoring β cell function by ...
Ruihan Li +5 more
wiley +1 more source
Novel drugs approved by the EMA, the FDA and the MHRA in 2025: A year in review
Abstract In the 2025 novel drug mini‐review, one can take a full measure of the ingenuity that underlies current drug design and development, despite the year's smaller harvest (46 novel drugs) compared to 2024 (53) and 2023 (70). 54% of the novel drugs are first‐in‐class (FIC).
Andreas Papapetropoulos +16 more
wiley +1 more source
Matrifibrocytes Redefine Cardiac Fibrosis: From Terminal Differentiation to Translational Modulation
ABSTRACT Cardiac fibrosis is increasingly recognized as a dynamic program that resolves into a terminal fibroblast fate, the matrifibrocyte, rather than a persistent myofibroblast state. Lineage‐tracing and single‐cell studies reveal that matrifibrocytes arise from activated myofibroblasts during late scar maturation, lose α‐SMA and proliferative ...
Zhentao Zhang, Hua Zhu
wiley +1 more source
Beneficial effects of SS-31 peptide on cardiac mitochondrial dysfunction in tafazzin knockdown mice
Barth Syndrome (BTHS), a genetic disease associated with early-onset cardioskeletal myopathy, is caused by loss-of-function mutations of the TAFAZZIN gene, which is responsible for remodeling the mitochondrial phospholipid cardiolipin (CL).
Silvia Russo +4 more
doaj +1 more source
BMAL1 Drives Cisplatin Resistance in Non‐Small Cell Lung Cancer Via Lactate‐MRP1 Signaling Pathway
The drug cisplatin induces BMAL1 expression through AKT signaling in response to cisplatin‐induced oxidative stress. BMAL1 activates HIF‐1α‐mediated metabolic reprogramming and lactate production, which in turn activates the TAZ/c‐Jun/Snail complex to upregulate drug efflux pump MRP1, initiating and sustaining chemoresistance. ABSTRACT Lung cancer, the
Zixin Shi +11 more
wiley +1 more source
Monolysocardiolipin in cultured fibroblasts is a sensitive and specific marker for Barth Syndrome
Barth Syndrome (BTHS) is an X-linked recessive disorder that results in abnormal metabolism of the mitochondrial phospholipid cardiolipin (CL). CLs are decreased and monolysocardiolipins (MLCLs), intermediates in CL metabolism, are increased in a variety
Michiel Adriaan van Werkhoven +3 more
doaj +1 more source
Barth Syndrome (BTHS) is a rare X-linked genetic disease caused by a mutation in the TAFAZZIN gene, which codes for the protein tafazzin involved in cardiolipin remodeling.
Hana M. Zegallai +2 more
doaj +1 more source

