Mesenchymal stem cells' "garbage bags" at work: Treating radial nerve injury with mesenchymal stem cell-derived exosomes.

Unlike central nervous system injuries, peripheral nerve injuries (PNIs) are often characterized by more or less successful axonal regeneration. However, structural and functional recovery is a senile process involving multifaceted cellular and molecular processes. The contemporary treatment options are limited, with surgical intervention as the gold-standard method; however, each treatment option has its associated limitations, especially when the injury is severe with a large gap.

Cellular preconditioning and mesenchymal stem cell ferroptosis.

In this editorial, we comment on the article published in the recent issue of the . They focus on stem cell preconditioning to prevent ferroptosis by modulating the cystathionine γ-lyase/hydrogen sulfide (HS) pathway as a novel approach to treat vascular disorders, particularly pulmonary hypertension. Preconditioned stem cells are gaining popularity in regenerative medicine due to their unique ability to survive by resisting the harsh, unfavorable microenvironment of the injured tissue.

AICAR Ameliorates Non-Alcoholic Fatty Liver Disease via Modulation of the HGF/NF-κB/SNARK Signaling Pathway and Restores Mitochondrial and Endoplasmic Reticular Impairments in High-Fat Diet-Fed Rats.

Non-alcoholic fatty liver disease (NAFLD) is a global health problem characterized by altered lipid and redox homeostasis, mitochondrial dysfunction, and endoplasmic reticulum (ER) stress. The AMP-dependent kinase (AMPK) agonist 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR) has been shown to improve the outcome of NAFLD in the context of AMPK activation, yet the underlying molecular mechanism remains obscure. This study investigated the potential mechanism(s) of AICAR to attenuate NAFLD by exploring AICAR's effects on the HGF/NF-κB/SNARK axis and downstream effectors as well as mitochondrial and ER derangements.

Alternative Chk1-independent S/M checkpoint in somatic cells that prevents premature mitotic entry.

Genomic instability is the hallmark of cancer. Checkpoint kinase-1 (Chk1) is required for cell cycle delay after DNA damage or blocked DNA replication. Chk1-depleted tumor cells undergo premature mitosis and apoptosis.

N-acetylcysteine a possible protector against indomethacin-induced peptic ulcer: crosstalk between antioxidant, anti-inflammatory, and antiapoptotic mechanisms.

This study investigated the gastroprotective effects of N-acetylcysteine (NAC) against indomethacin-induced gastric ulcer in rats. Ulceration was induced by a single oral administration of indomethacin (30 mg/kg). 50 male albino rats were allocated into 5 equal groups: control group received normal saline orally, indomethacin group rats received normal saline orally for 5 days and indomethacin (50 mg/kg) on the last day, ranitidine group received ranitidine (reference drug) orally for 5 days (50 mg/kg) before receiving indomethacin (50 mg/kg) on the last day, and NAC groups received NAC orally at 300 and 500 mg/kg, respectively, for 5 days before receiving indomethacin (50 mg/kg) on the last day.

Sucrose non-fermenting AMPK related kinase/Pentraxin 3 and DNA damage axis: a gateway to cardiovascular disease in systemic lupus erythematosus among Egyptian patients.

Background: Systemic lupus erythematosus is a chronic multisystemic autoimmune disease characterized by chronic inflammatory processes and failure of immune-regulatory mechanisms. Systemic lupus erythematosus is associated with increased risk for cardiovascular disease. In view of immunometabolic derangements of systemic lupus erythematosus, we investigated the roles of sucrose non-fermenting AMPK related kinase, Pentraxin 3, and DNA damage in the pathogenesis of systemic lupus erythematosus complicated with cardiovascular disease.

Fatty acid synthase/oxidized low-density lipoprotein as metabolic oncogenes linking obesity to colon cancer via NF-kappa B in Egyptians.

Obesity is a major health problem which heightens the risk of several chronic illnesses including cancer development particularly colon cancer. The underlying pathophysiology of obesity associated colon cancer remains to be elucidated. The purpose of this current study was to determine fatty acid synthase (FASN) activity/expression, oxidized low-density lipoprotein (ox-LDL) level and redox status under the context of anthropometric measurements and lipid profile to find their potential role as interacting biomarkers relating obesity to colon cancer initiation and progression via nuclear factor kappa-B (NF-κB) signaling.

Effect of NUCKS-1 overexpression on cytokine profiling in obese women with breast cancer.

Background: Overweight and obesity are recognized as major drivers of cancers including breast cancer. Several cytokines, including interleukin-6 (IL-6), IL-10 and lipocalin 2 (LCN2), as well as dysregulated cell cycle proteins are implicated in breast carcinogenesis. The nuclear, casein kinase and cyclin-dependent kinase substrate-1 (NUCKS-1), is a nuclear DNA-binding protein that has been implicated in several human cancers, including breast cancer.

NF-kappa B signature on the aging wall.

During the lifetime, our cells encounter many challenges to their own existence. The survival of organisms and cells depends on the interplay within a complex, yet precisely orchestrated network of proteins. Since the discovery of the Rel/NF-kappaB family of transcription factors, the research has never come to a stop.