Results 171 to 180 of about 282,340 (392)
Basic fibroblast growth factor from human keratinocytes is a natural mitogen for melanocytes. [PDF]
Ruth Halaban +7 more
openalex +1 more source
ObjectiveTherapeutic angiogenesis is an alternative method of revascularization for end-stage coronary artery disease. We determined the effects of intramyocardial and intracoronary basic fibroblast growth factor 2 on myocardial blood flow and function ...
Smith, Monica L +19 more
core +1 more source
A genome‐wide microRNA CRISPR screen identifies miR‐18a as a master regulator of cross‐resistance in melanoma. Loss of miR‐18a activates the AJUBA–YAP/Hippo axis to confer BRAFi resistance and enhances THBS1–CD47 interaction to impair CD8+ T cell immunity. hnRNP A1 is identified as an upstream regulator of miR‐18a processing.
Zhao Wang +19 more
wiley +1 more source
This study established an RT‐MSCs‐based therapeutic approach for scleroderma in mice. RT‐MSCs attenuated fibrosis by regulating mitochondrial autophagy and restored gut microbiota homeostasis. Metabolomic analyses confirmed recovery of key metabolites, and RT‐MSCs demonstrated favorable lesion targeting and safety profiles.
Xue Xia +5 more
wiley +1 more source
Cerebral intraventricular infusion of acidic or basic fibroblast growth factor has been shown to attenuate ischemic damage to hippocampal CA1 neurons in the gerbil.
A Wiseman +5 more
core +1 more source
DOT1L as a central epigenetic regulator of EndoMT and pulmonary fibrosis. Acting as an early epigenetic switch, it translates TGFβ–SMAD signaling into H3K79me2‐mediated chromatin remodeling, selectively activates fibrosis‐related genes, and primes ECs for rapid mesenchymal transition.
Yaofeng Wang +11 more
wiley +1 more source
Targeting the PDK1/c‐Myc/SOX10 Signaling in Oligodendrocytes Alleviates Neuropathic Pain
This work reveals that oligodendrocyte homeostasis, mediated by PDK1, is a critical determinant of neuropathic pain (NPP) pathogenesis. Disruption of PDK1 in oligodendrocytes impairs SOX10‐dependent myelination programs through c‐Myc accumulation, leading to disrupted myelination and the pathophysiology of NPP.
Pingping Qiao +7 more
wiley +1 more source

