Results 191 to 200 of about 2,432,790 (318)

Cyclic azapeptide CD36 ligand attenuates cardiac injury and reduces long‐chain fatty acid accumulation after myocardial ischemia–reperfusion in mice

open access: yesFEBS Open Bio, EarlyView.
In a murine model of myocardial ischemia and reperfusion (MI/R), the CD36 azapeptide ligand MPE‐298 reduces cardiac injury and transiently lowers left ventricular long‐chain fatty acids (LCFAs) accumulation 3 h after reperfusion, accompanied by a decrease of oxidative stress and inflammation‐associated genes' expression in the heart and adipose tissue.
Jade Gauvin   +12 more
wiley   +1 more source

Non-governmental organisations and the regulation of harmful commodity industries: navigating global governance to change corporate practices. [PDF]

open access: yesGlobal Health
Lauber K   +9 more
europepmc   +1 more source

Emerging insights into CC and CXC chemokines and their receptors in Mycobacterium tuberculosis infection

open access: yesFEBS Open Bio, EarlyView.
The dual roles of CC and CXC chemokines in distinguishing active, latent, and subclinical tuberculosis were reviewed, along with an evaluation of their potential as diagnostic biomarkers and therapeutic targets to advance precision medicine in tuberculosis management. The graphical abstract was generated with AI assistance (Gemini 3.0).
Xuying Yin, Dangsheng Xiao, Jiezuan Yang
wiley   +1 more source

Natural Products as Geroprotective Modulators in Diabetic Nephropathy: A Mechanistic Framework Integrating Aging Hallmarks and the AMPK–SIRT1–Nrf2 Axis

open access: yesAging and Cancer, EarlyView.
Natural products target the aging kidney in diabetic nephropathy by restoring the AMPK–SIRT1–Nrf2 axis, reducing oxidative stress, inflammation, fibrosis, and cellular senescence while enhancing mitochondrial biogenesis and antioxidant defenses.
Sherif Hamidu   +8 more
wiley   +1 more source

Mutant NPM1 in Acute Myeloid Leukemia Initiation and Maintenance

open access: yesAging and Cancer, EarlyView.
NPM1 mutations drive acute myeloid leukemia by acting as neomorphic transcriptional regulators that cooperate with Menin–MLL and XPO1 to sustain HOX/MEIS1 expression and block differentiation. Targeting these mutant‐specific transcriptional dependencies provides a rational therapeutic strategy for NPM1‐mutated AML.
Yanan Jiang   +3 more
wiley   +1 more source

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