Lipocalin-2 induces mitochondrial dysfunction in renal tubular cells via mTOR pathway activation.

Mitochondrial dysfunction is a critical process in renal epithelial cells upon kidney injury. While its implication in kidney disease progression is established, the mechanisms modulating it remain unclear. Here, we describe the role of Lipocalin-2 (LCN2), a protein expressed in injured tubular cells, in mitochondrial dysfunction.

Cholecalciferol (vitamin D) has a direct protective activity against interleukin 6-induced atrophy in C2C12 myotubes.

We previously determined that different vitamin D metabolites can have opposite effects on C2C12 myotubes, depending on the sites of hydroxylation or doses. Specifically, 25(OH)D (25VD) has an anti-atrophic activity, 1,25(OH)D induces atrophy, and 24,25(OH)D is anti-atrophic at low concentrations and atrophic at high concentrations. This study aimed to clarify whether cholecalciferol (VD3) too, the non-hydroxylated upstream metabolite, has a direct effect on muscle cells.

Both ghrelin deletion and unacylated ghrelin overexpression preserve muscles in aging mice.

Sarcopenia, the decline in muscle mass and functionality during aging, might arise from age-associated endocrine dysfunction. Ghrelin is a hormone circulating in both acylated (AG) and unacylated (UnAG) forms with anti-atrophic activity on skeletal muscle. Here, we show that not only lifelong overexpression of UnAG (Tg) in mice, but also the deletion of ghrelin gene ( KO) attenuated the age-associated muscle atrophy and functionality decline, as well as systemic inflammation.

Opposing effects of 25-hydroxy- and 1α,25-dihydroxy-vitamin D on pro-cachectic cytokine-and cancer conditioned medium-induced atrophy in C2C12 myotubes.

Aim: Loss of skeletal muscle is one of the main features of cancer cachexia. Vitamin D (VD) deficiency is associated with impairment of muscle mass and performance and is highly prevalent in cachectic patients; therefore, VD supplementation has been proposed to counteract cancer cachexia-associated muscle loss. However, in both cachectic cancer patients and tumour-bearing animals, VD supplementation led to disappointing results, urging the need for a better understanding of VD activity on skeletal muscle.

Role of regulatory T cells in irinotecan-induced intestinal mucositis.

Intestinal mucositis (IM) is a common side effect of irinotecan-based chemotherapy. The involvement of inflammatory mediators, such as TNF-α, IL1-β, IL-18 and IL-33, has been demonstrated. However, the role of adaptive immune system cells, whose activation is partially regulated by these cytokines, is yet unknown.