Results 201 to 210 of about 27,445 (272)

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

Inositol phosphates and phosphoinositides activate insulin-degrading enzyme, while phosphoinositides also mediate binding to endosomes. [PDF]

open access: yesProc Natl Acad Sci U S A, 2017
Song ES   +8 more
europepmc   +1 more source

A role for epithelium‐derived 6‐nitrodopamine on human ureter contractility

open access: yesBritish Journal of Pharmacology, Volume 183, Issue 10, Page 2360-2375, May 2026.
Abstract Background and Purpose To investigate the basal release of 6‐nitrodopamine (6‐ND) from human isolated ureter and the role of this novel catecholamine in the ureter contractility. Experimental Approach Ureters from 67 brain‐dead organ donors (40 males and 27 females) were used during kidney transplantation procedures.
Wilmar Azal Neto   +12 more
wiley   +1 more source

Ageing‐Dependent Thyroid Hormone Receptor α Reduction Activates IP3R1‐Meditated Ca2+ Transfer in MAM and Exacerbates Skeletal Muscle Atrophy in Mice

open access: yesCell Proliferation, Volume 59, Issue 5, May 2026.
During skeletal muscle ageing, down‐regulation of TRα expression activates IP3R1 transcriptional expression, promotes MAM calcium transport, triggers mitochondrial calcium overload and apoptosis, leading to skeletal muscle atrophy. Restoring TRα expression can improve IP3R1‐mediated mitochondrial calcium overload and apoptosis in ageing skeletal muscle
Runqing Shi   +7 more
wiley   +1 more source

Fibrinogen - a possible extracellular target for inositol phosphates. [PDF]

open access: yesMessenger (Los Angel), 2012
Grint T   +4 more
europepmc   +1 more source

Emerging Role of Ferroptosis in Diabetes and Associated Complications: When Metabolic Dysregulation Meets Cell Death

open access: yesCell Proliferation, Volume 59, Issue 5, May 2026.
This study identifies ferroptosis as a key driver of diabetes and its complications via iron metabolism and lipid peroxidation, elucidates organelle interactions underlying cell vulnerability, and provides insights for targeted therapies against metabolic disorders.
Zheng Wang   +10 more
wiley   +1 more source

Regulation of Endoplasmic Reticulum Stress by Empagliflozin in Doxorubicin‐Induced Cardiotoxicity in Rats

open access: yesJournal of Cellular and Molecular Medicine, Volume 30, Issue 9, May 2026.
ABSTRACT Although Doxorubicin (Dox) is an effective anticancer drug, it can cause severe cardiotoxicity. While several mechanisms have been proposed to explain Dox‐induced cardiomyopathy (DIC), strategies to prevent it remain limited. In previous research on isolated cardiomyocytes, we identified that Empagliflozin (EMPA), an antidiabetic drug ...
Akshi Malik   +6 more
wiley   +1 more source

Chromaffin Versus Platelet Granules: What We Have Learned From Chromaffin Cells for Human Studies

open access: yesJournal of Neurochemistry, Volume 170, Issue 5, May 2026.
Chromaffin cells and platelets both utilize exocytosis to release biogenic amines stored within large dense‐core vesicles—specifically chromaffin granules (epinephrine) and δ‐granules (serotonin). While the chromaffin cell is the foundational model for studying the secretory pathway, platelets offer a highly accessible human cell source for clinical ...
Ricardo Borges
wiley   +1 more source

Defining signal transduction by inositol phosphates. [PDF]

open access: yesSubcell Biochem, 2012
Shears SB   +7 more
europepmc   +1 more source

Epigenetic analyses suggest different pathways during pregnancy for development of type 1 diabetes in children with high versus low‐neutral human leukocyte antigen‐risk

open access: yesJournal of Internal Medicine, Volume 299, Issue 5, Page 570-586, May 2026.
Abstract Background and objective The development of Type 1 diabetes (T1D) is shaped by genetic predisposition and epigenetic regulation. Human leukocyte antigen (HLA) risk alleles are major genetic determinants, but the epigenetic landscape in relation to disease onset remains unclear.
Shamila D. Alipoor   +6 more
wiley   +1 more source

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