Results 61 to 70 of about 2,732 (148)
Matrifibrocytes Redefine Cardiac Fibrosis: From Terminal Differentiation to Translational Modulation
Journal 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
Deletion of Tafazzin in Cardiomyocytes Results in Dilated Cardiomyopathy [PDF]
, 2020 Cardiolipin, the signature phospholipid of mitochondria, is crucial for mitochondrial function and architecture in the heart. Defects in cardiolipin remodeling processes and metabolism lead to cardiomyopathy, as seen in patients with Barth Syndrome (BTHS)
Zhu, Mason
core +1 more source
Scientific ReportsBarth 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
Substantial Decrease in Plasmalogen in the Heart Associated with Tafazzin Deficiency
, 2018 Tafazzin is the mitochondrial enzyme that catalyzes transacylation between a phospholipid and a lysophospholipid in remodeling. Mutations in tafazzin cause Barth syndrome, a potentially life-threatening disease with the major symptom being cardiomyopathy.
Yang Xu (178421) +6 more
core +1 more source
, 2022 Tafazzin—an acyltransferase—is involved in cardiolipin (CL) remodeling. CL is associated with mitochondrial function, structure and more recently with cell proliferation. Various tafazzin isoforms exist in humans.
Michael Linnebacher (180341) +11 more
core +1 more source
Scientific ReportsBarth 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
Deficiency in Cardiolipin Reduces Doxorubicin-Induced Oxidative Stress and Mitochondrial Damage in Human B-Lymphocytes. [PDF]
PLoS ONE, 2016 Cardiolipin (CL) is an inner mitochondrial membrane phospholipid which plays an important role in mitochondrial function. Perturbation in CL biosynthesis alters mitochondrial bioenergetics causing a severe genetic disorder commonly known as Barth ...
Baikuntha Aryal, V Ashutosh Rao
doaj +1 more source
BMAL1 Drives Cisplatin Resistance in Non‐Small Cell Lung Cancer Via Lactate‐MRP1 Signaling Pathway
Thoracic 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
, 2022 Tafazzin—an acyltransferase—is involved in cardiolipin (CL) remodeling. CL is associated with mitochondrial function, structure and more recently with cell proliferation. Various tafazzin isoforms exist in humans.
Michael Linnebacher (180341) +11 more
core +1 more source
British 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