Results 41 to 50 of about 2,310 (125)

Mitochondrial Homeostasis in Pancreatic β Cell Function: Mechanisms and Therapeutic Targets for Diabetes

open access: yesJournal of Diabetes, Volume 18, Issue 5, May 2026.
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

open access: yesBritish Journal of Pharmacology, Volume 183, Issue 9, Page 1779-1813, May 2026.
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

Stimulating myocardial pyruvate dehydrogenase activity fails to alleviate cardiac abnormalities in a mouse model of human Barth syndrome

open access: yesFrontiers in Cardiovascular Medicine, 2022
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

Matrifibrocytes Redefine Cardiac Fibrosis: From Terminal Differentiation to Translational Modulation

open access: yesJournal of Cellular and Molecular Medicine, Volume 30, Issue 10, May 2026.
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

Thematic Review Series: Glycerolipids. Cardiolipin synthesis for the assembly of bacterial and mitochondrial membranes*

open access: yesJournal of Lipid Research, 2008
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

Beneficial effects of SS-31 peptide on cardiac mitochondrial dysfunction in tafazzin knockdown mice

open access: yesScientific Reports, 2022
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

open access: yesThoracic Cancer, Volume 17, Issue 8, April 2026.
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

Upregulation of the AMPK-FOXO1-PDK4 pathway is a primary mechanism of pyruvate dehydrogenase activity reduction in tafazzin-deficient cells

open access: yesScientific Reports
Barth syndrome (BTHS) is a rare disorder caused by mutations in the TAFAZZIN gene. Previous studies from both patients and model systems have established metabolic dysregulation as a core component of BTHS pathology.
Zhuqing Liang   +12 more
doaj   +1 more source

Expanding genetic landscape of inherited bone marrow failure syndromes: Insights from the Canadian Inherited Marrow Failure Registry (CIMFR) (2001–2023)

open access: yesBritish Journal of Haematology, Volume 208, Issue 4, Page 1407-1418, April 2026.
Summary Inherited bone marrow failure syndromes (IBMFSs) are genetically heterogeneous with an expanding spectrum of causative genes. Recent molecular advances are thought to have contributed to genetic identification, yet the true gain in diagnostic yield remains unclear.
Ye Jee Shim   +21 more
wiley   +1 more source

SS-31 treatment ameliorates cardiac mitochondrial morphology and defective mitophagy in a murine model of Barth syndrome

open access: yesScientific Reports
Barth syndrome (BTHS) is a lethal rare genetic disorder, which results in cardiac dysfunction, severe skeletal muscle weakness, immune issues and growth delay.
Silvia Russo   +4 more
doaj   +1 more source

Home - About - Disclaimer - Privacy