Results 221 to 230 of about 954,264 (289)

Renal involvement in Fabry disease from Tunisian families: Six case reports. [PDF]

open access: yesWorld J Nephrol
Tlili S   +5 more
europepmc   +1 more source

A Contemporary Pathomechanistic Nosology of Inherited Lysosomal Disorders. [PDF]

open access: yesJ Inherit Metab Dis
McCarron EP   +7 more
europepmc   +1 more source

α-Mangostin attenuates <i>Pseudomonas aeruginosa</i> virulence by targeting PqsR and inhibiting PQS-mediated quorum sensing. [PDF]

open access: yesVirulence
Liu D   +12 more
europepmc   +1 more source

Mechanism of action of alpha-galactosidase.

open access: yesIndian journal of biochemistry & biophysics, 1988
C D, Mathew, K, Balasubramaniam
openaire   +1 more source

PLL‐g‐HPA Hydrogel Microneedles Loaded With Rhoifolin Target Macrophages to Alleviate Fibroblast Senescence for Diabetic Wound Healing

open access: yesAdvanced Healthcare Materials, Volume 15, Issue 38, 16 October 2026.
Diabetic wound healing is hindered by a pathological crosstalk wherein elevated IL‐11 induces M1 macrophage polarization, leading to IL‐1β/IL‐6 release and subsequent fibroblast senescence via RAS/p38MAPK/p53/E2F1 signaling. Here, we develop a Gel@M‐Rho microneedle patch that delivers rhoifolin‐loaded, macrophage membrane‐coated nanoparticles to target
Jiewen Liao   +10 more
wiley   +1 more source

HMGCR‐Driven Cholesterol Metabolism Promotes Osteoarthritis Progression by Accelerating Synovial Fibroblast Senescence

open access: yesAdvanced Science, Volume 13, Issue 55, 5 October 2026.
In the pathological context of osteoarthritis (OA), the phosphorylation of AKT1 at Ser473 enhances its binding to Lys140 of Insig1, which facilitates the formation of AKT1–Insig1 complex. Subsequently, the activation of AKT1 promotes the phosphorylation of Insig1 at Ser189, potentially enhancing the dissociation of Insig1 from sterol regulatory element‑
Xiaoqi Zhang   +19 more
wiley   +1 more source

TPI1 Loss Triggers a Metabolite‐Driven Mitochondrial Redox Vulnerability via the SARM1–cADPR–Ca2+ Axis

open access: yesAdvanced Science, Volume 13, Issue 56, 9 October 2026.
Metabolite‐driven redox stress governs cancer cell senescence. TPI1 deficiency elevates DHAP, initiating SARM1‐dependent cADPR‐Ca2+ release. Mitochondrial ROS surge subsequently induces DNA damage and senescence, offering a conserved therapeutic target in multiple cancers.
Chunyu Liu   +15 more
wiley   +1 more source

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