Cancer associated fibroblasts (CAFs) are the main stromal cell type of solid tumour microenvironment and undergo an activation process associated with secretion of growth factors, cytokines, and paracrine interactions. One of the important features of solid tumours is the metabolic reprogramming that leads to changes of bioenergetics and biosynthesis in both tumour cells and CAFs. In particular, CAFs follow the evolution of tumour disease and acquire a catabolic phenotype: in tumour tissues, cancer cells and tumour microenvironment form a network where the crosstalk between cancer cells and CAFs is associated with cell metabolic reprogramming that contributes to CAFs activation, cancer growth, and progression and evasion from cancer therapies. In this regard, the study of CAFs metabolic reprogramming could contribute to better understand their activation process, the interaction between stroma, and cancer cells and could offer innovative tools for the development of new therapeutic strategies able to eradicate the protumorigenic activity of CAFs. Therefore, this review focuses on CAFs metabolic reprogramming associated with both differentiation process and cancer and stromal cells crosstalk. Finally, therapeutic responses and potential anticancer strategies targeting CAFs metabolic reprogramming are reviewed.

Tendinopathies are very common in general population and a huge number of tendon-related procedures take place annually worldwide, with significant socio-economic repercussions. Numerous treatment options are commonly used for tendon disorders. Besides pharmacological and physical therapy, nutrition could represent an additional tool for preventing and treating this complex pathology that deserve a multidisciplinary approach. In recent years, nutraceutical products are growing up in popularity since these seem to favor the prevention and the healing processes of tendon injuries. This narrative literature review aims to summarize current understanding and the areas of ongoing research about the management of tendinopathies with the help of oral supplementation.

Cardiac tissue engineering by means of synthetic or natural scaffolds combined with stem/progenitor cells is emerging as the response to the unsatisfactory outcome of approaches based solely on the injection of cells. Parenchymal and supporting cells are surrounded, in vivo, by a specialized and tissue-specific microenvironment, consisting mainly of extracellular matrix (ECM) and soluble factors incorporated in the ECM. Since the naturally occurring ECM is the ideal platform for ensuring cell engraftment, survival, proliferation, and differentiation, the acellular native ECM appears by far the most promising and appealing substrate among all biomaterials tested so far. To obtain intact scaffold of human native cardiac ECM while preserving its composition, we compared the decellularized ECM (d-ECM) produced through five different protocols of decellularization (named Pr1, Pr2, Pr3, Pr4, and Pr5) in terms of efficiency of decellularization, composition, and three-dimensional architecture of d-ECM scaffolds and of their suitability for cell repopulation. The decellularization procedures proved substantially different. Specifically, only three, of the five protocols tested, proved effective in producing thoroughly acellular d-ECM. In addition, the d-ECM delivered differed in architecture and composition and, more importantly, in its ability to support engraftment, survival, and differentiation of cardiac primitive cells in vitro.

Breast cancers are very heterogeneous tissues with several cell types and metabolic pathways together sustaining the initiation and progression of disease and contributing to evasion from cancer therapies. Furthermore, breast cancer cells have an impressive metabolic plasticity that is regulated by the heterogeneous tumour microenvironment through bidirectional interactions. The structure and accessibility of nutrients within this unstable microenvironment influence the metabolism of cancer cells that shift between glycolysis and mitochondrial oxidative phosphorylation (OXPHOS) to produce adenosine triphosphate (ATP). In this scenario, the mitochondrial energetic pathways of cancer cells can be reprogrammed to modulate breast cancer’s progression and aggressiveness. Moreover, mitochondrial alterations can lead to crosstalk between the mitochondria and the nucleus, and subsequently affect cancer tissue properties. This article reviewed the metabolic plasticity of breast cancer cells, focussing mainly on breast cancer mitochondrial metabolic reprogramming and the mitochondrial alterations influencing nuclear pathways. Finally, the therapeutic strategies targeting molecules and pathways regulating cancer mitochondrial alterations are highlighted.