CD36 functions as both a lipid transporter and scavenger receptor, integrating metabolic and inflammatory signaling pathways. It plays a critical role in maintaining cellular homeostasis and influencing disease progression. This review summarizes the structure, ligands, functions, regulation, and clinical implications of CD36 in renal and bladder cancer. Increased CD36 expression promotes enhanced fatty acid uptake, which supports tumor cell proliferation, migration and survival, by mediating metabolic reprogramming and interacting with the tumor microenvironment. In renal cancer, most frequently clear cell renal carcinoma (ccRCC), which has a typical metabolic phenotype, CD36 is involved in lipid accumulation and oxidative stress pathways. Pathogenic mechanisms include hypoxia-inducible factor (HIF)-driven pathways and carnitine palmitoyl transferase 1A (CPT1A) via the PPARα/CD36 axis, which phosphorylate Akt. By using fatty acid oxidation, CD36 lead to the production of reactive oxygen species and to transcription of genes mediating a pro-tumor function, inducing tumor-associated macrophages (TAM). In bladder cancer, CD36 is implicated in tumoral cells proliferation, survival, and adaptation to metabolic stress, epithelial-mesenchymal transition (EMT) and influences the tumor microenvironment, through interactions with tumor-associated macrophages and inflammatory signaling pathways. Although multiple studies propose CD36 as a prognostic biomarker, inconsistencies across cohorts limit its clinical translation. Notably, advances have revealed the regulatory networks governing distinct physiological properties of CD36, thereby identifying targeting CD36 as a potential strategy for cancer treatment. Inhibition of CD36-mediated lipid metabolism and signaling pathways may reduce tumor growth and metastatic potential. However, further research is necessary to clarify its context-dependent functions and to develop effective CD36-targeted therapies. To our knowledge, this is the first review to systematically examine the role of CD36 across both renal and bladder cancer. It could be the first step toward identifying new mechanisms mediated by CD36 in these malignancies.

Psychotic disorders are a group of severe psychiatric conditions with onset typically occurring in adolescence or early adulthood. Despite significant efforts to identify clinically useful candidates, no validated biomarkers for psychiatric disorders currently exist. The diagnosis of psychotic disorders is exclusively based on clinical assessment, significantly affected by individual differences and symptom overlap. Although circulating microRNAs (miRNAs) have emerged as potential peripheral biomarkers for early diagnosis and disease evolution, most studies concentrate on adult, medicated cohorts. Studies on miRNA profiles in drug-naïve adolescents with first-episode psychosis (FEP) are scarce. This study aims to identify the plasma miRNA profile in treatment-naïve Romanian adolescents with first-episode psychosis and to compare it with that of age- and sex-matched healthy controls. The plasma from 14 adolescents, seven drug-naïve FEP and seven and age-matched controls (CTRL) aged 15–18 years was collected. Psychiatric symptoms were assessed using PANSS, HAM-D, and YMRS scales. The levels of 179 miRNAs were assessed using qRT-PCR. A case-control analysis on miRNAs levels between FEP and CTRL was performed, as well as correlations with clinical measures. Twenty-one miRNAs showed significantly lower levels and two higher levels in FEP patients compared to controls. After adjustment for multiple comparisons, miR-125a-5p, miR-205-5p, miR-145-5p, miR-363-3p, and miR-23b-3p remained statistically significant (FDR<0.05). Notably, miR-125a-5p, miR-23b-3p, and miR-146a-5p levels negatively correlated with psychotic, depressive, and manic symptom severity, while miR-16-5p and miR-363-3p positively correlated with symptom scores. Comparison with previous studies indicated limited overlap, reflecting potential influences of age, treatment status, and genetic or environmental factors. This work demonstrates that Romanian treatment-naïve adolescents with first-episode psychosis had a unique circulating miRNA profile correlated with symptom severity, indicating their potential as early-stage biomarkers. The results underscore the necessity of accounting for age, treatment status, and environmental variables in the interpretation of miRNA modifications in psychotic illnesses.

Background: Bladder cancer remains a heterogeneous disease, and genetic factors are increasingly recognized as potential contributors to its pathogenesis. CD36, a multifunctional scavenger receptor implicated in lipid metabolism and tumor progression, has not been previously investigated in relation to bladder cancer-associated polymorphisms. Objectives: This study examined the relationship between the rs1761667 variant and CD36 mRNA expression. Methods: Our study included 30 patients with bladder cancer and 19 controls. PCR–RFLP genotyping for rs1761667 and RT–qPCR quantification of CD36 mRNA expression, with GAPDH as the reference gene, were performed. Expression levels were analyzed using the 2−ΔΔCt method, and statistical significance was defined as p < 0.05. Results: In patients, CD36 expression varied significantly across rs1761667 genotypes with reduced expression in AA carriers compared with GG carriers (post hoc, p = 0.009, with a Holm-adjusted p = 0.03). No significant genotype-related differences were observed among controls. Genotype distributions did not differ significantly between cases and controls (χ2, p = 0.053). Conclusions: These results indicate that rs1761667 may modulate CD36 transcription in a genotype-dependent manner, particularly in the disease context. Overall, our findings point to a potential biological connection between inherited CD36 variation and bladder cancer-related pathways, underscoring the need for further validation in tumor tissues

Colorectal cancer (CRC) continues to represent a substantial worldwide health burden. Accurate risk classification and early detection have a significant impact on prognosis. There is still a significant percentage of patients who are diagnosed at advanced stages, notwithstanding the progress that has been made in screening and treatment. Thus, improved molecular tools that encompass the biological complexity of CRC are needed. High-throughput technologies have expanded the biomarker array for CRC screening, prognosis, and therapeutic prediction. This review summarizes evidence on established and emerging molecular tools from tumor tissue, blood, and stool samples, such as DNA mutations, methylation markers, RNA signatures, circulating tumor DNA (ctDNA), circulating cell-free DNA (cfDNA), extracellular vesicles, and multi-omic composite assays. These provide alternatives to conventional approaches that are relatively less invasive and more sensitive. Prognostic biomarkers—such as RAS, BRAF, HER2 alterations, mismatch repair deficiency, tumor mutational burden, methylation signatures, and non-coding RNAs—provide insight into tumor behavior and recurrence risk. To guide targeted therapies, immunotherapies, and chemotherapy response, predictive biomarkers such as RAS/BRAF mutations, HER2 amplification, MSI-H/dMMR status, POLE/POLD1 mutations, DNA methylation panels, miRNAs, lncRNAs, and liquid biopsy markers are crucial. Emerging technologies such as multi-omics, AI-enhanced biomarker discovery, and novel liquid biopsy components (evDNA, circRNAs) pave the way to precision oncology. These molecular tools have the potential to change how CRC is managed by earlier detection and more precise predictive biomarkers. However, large-scale validation and clinical standardization are still crucial for their extensive utilization.

CD36 is a multifunctional scavenger receptor involved in long-chain fatty acid (LCFA) uptake, binding of oxidized lipids, and interactions with extracellular matrix proteins such as thrombospondin-1. Through association with Src family kinases, integrins, and adaptor proteins, it also modulates signaling, migration, inflammation, angiogenesis, and phagocytosis. Hypoxia, a common feature of solid tumors, inflamed tissues, and ischemic organs, remodels CD36 expression, localization, and function through hypoxia-inducible factor (HIF) signaling and stress-activated kinases. These effects change cellular metabolism, intercellular lipid trafficking, and cell behavior (migration, phagocytosis, angiogenesis, immune phenotype) in a manner that is highly dependent on tissue type, duration of hypoxia, and metabolic context, with important implications for disease progression. In acute hypoxia, CD36 regulation often contributes to rapid metabolic adaptation, whereas in chronic hypoxia, it may promote sustained lipid accumulation, inflammation, maladaptive remodeling, or tumor progression. In this review, we aim to highlight the regulation and function of CD36 in hypoxia in different tissues, conditions, and metabolic states, emphasizing the distinct roles of CD36 in acute versus chronic hypoxia and its potential therapeutic implications. For example, hypoxia typically downregulates CD36 in ischemic cardiomyocytes to limit lipotoxic fatty acid influx, whereas in hepatocytes, adipocytes, and tumor-associated macrophages, it upregulates CD36-mediated lipid uptake to sustain steatotic, inflammatory, or protumorigenic metabolism, illustrating the tissue-specific nature of this regulation.

BACKGROUND:Colorectal cancer (CRC) is one of the most common cancers worldwide. The gold standard screening methods for early detection and monitoring are colonoscopy and stool-based tests. However, innovative and minimally invasive biomarkers need to be integrated into clinical practice. AIM:To identify circulating microRNAs as potential CRC biomarkers through a comparative analysis of tissue and plasma samples from patients with CRC. METHODS:This case-control study conducted a quantitative real-time polymerase chain reaction analysis of 84 microRNAs in tumoral and peritumoral tissues, and 179 microRNAs in plasma from 19 patients with CRC. A control cohort for the tissue analysis and another control cohort for the plasma analysis have been enrolled. RESULTS:In total, 14 microRNAs were significantly differentially expressed in the tissue and plasma samples. Notably, five microRNAs (miR-26b-5p, miR-101-3p, miR-30d-5p, miR-107, and miR-21-5p) presented the same trend in terms of fold change in both types of biological samples. Significant associations between the circulating levels of miR-21-5p and miR-26b-5p and lymphovascular invasion were found. CONCLUSION:These five microRNAs with significantly altered levels in plasma and tumoral tissue, could be good non-invasive CRC biomarkers candidates, enhancing screening, and supporting precision and individualized patient care.

BACKGROUND:Pancreatic ductal adenocarcinoma (PDAC) is an aggressive lethal malignancy with limited options for treatment and a 5-year survival rate of 11% in the United States. As for other types of tumors, such as colorectal cancer, aberrant de novo lipid synthesis and reprogrammed lipid metabolism have been suggested to be associated with PDAC development and progression. AIM:To identify the possible involvement of lipid metabolism in PDAC by analyzing in tumoral and non-tumoral tissues the expression level of the most relevant genes involved in the long-chain fatty acid (FA) import into cell. METHODS:A gene expression analysis of FASN, CD36, SLC27A1, SLC27A2, SLC27A3, SLC27A4, SLC27A5, ACSL1, and ACSL3 was performed by qRT-PCR in 24 tumoral PDAC tissues and 11 samples from non-tumoral pancreatic tissues obtained via fine needle aspiration or via surgical resection. The genes were considered significantly dysregulated between the groups when the p value was < 0.05 and the fold change (FC) was ≤ 0.5 and ≥ 2. RESULTS:We found that three FA transporters and two long-chain acyl-CoA synthetases genes were significantly upregulated in the PDAC tissue compared to the non-tumoral tissue: SLC27A2 (FC = 5.66; P = 0.033), SLC27A3 (FC = 2.68; P = 0.040), SLC27A4 (FC = 3.13; P = 0.033), ACSL1 (FC = 4.10; P < 0.001), and ACSL3 (FC = 2.67; P = 0.012). We further investigated any possible association between the levels of the analyzed mRNAs and the specific characteristics of the tumors, including the anatomic location, the lymph node involvement, and the presence of metastasis. A significant difference in the expression of SLC27A3 (FC = 3.28; P = 0.040) was found comparing patients with and without lymph nodes involvement with an overexpression of this transcript in 17 patients presenting tumoral cells in the lymph nodes. CONCLUSION:Despite the low number of patients analyzed, these preliminary results seem to be promising. Addressing lipid metabolism through a broad strategy could be a beneficial way to treat this malignancy. Future in vitro and in vivo studies on these genes may offer important insights into the mechanisms linking PDAC with the long-chain FA import pathway.

Prostate cancer, a malignancy of significant prevalence, affects approximately half a million men in Europe, with one in twelve males receiving a diagnosis before reaching the age of 75. Radiotheranostics represents a paradigm shift in prostate cancer treatment, leveraging radionuclides for diagnostic and therapeutic applications, with PSMA emerging as the primary molecular target. Regulatory bodies have approved various PSMA-targeted radiodiagnostic agents, such as [18F]DCFPyL (PYLARIFY®, Lantheus Holdings), [18F]rhPSMA-7.3 (POSLUMA®, Blue Earth Diagnostics), and [68Ga]Ga-PSMA-11 (LOCAMETZ®, Novartis/ILLUCCIX®, Telix Pharmaceuticals), as well as therapeutic agents like [177Lu]Lu-PSMA-617 (PLUVICTO®, 15 Novartis). The approval of PLUVICTO® in March 2022 for patients with metastatic castration-resistant prostate cancer who have undergone prior treatments, including androgen receptor pathway-targeting agents and taxane-based chemotherapy, represents a significant advancement. Other radionuclides like 161Tb, 149Tb, 225Ac, 227Th, 223Ra, 211At, 213 Bi, 212Pb, 89Zr, and 125I are presented, emphasizing their clinical implementation or the stage of clinical trial they are in in the flow to biomedical implementation. Three clinically wise used radionuclides 177Lu, 225Ac, 223Ra are shown along with their characteristics. This review aims to elucidate the molecular mechanisms underpinning PSMA, explore the clinical applications of PSMA-targeted radiotheranostics, and critically examine the diverse challenges these therapies encounter in the treatment of prostate cancer.

Autism spectrum disorders (ASDs) are neurodevelopmental conditions characterized by important clinical and genetic heterogeneity. Recent studies suggested an overlap between ASD and Parkinson's disease (PD) in terms of clinical manifestation and underlying genetic defects. Our aim was to assess using a chromosomal microarray assay the frequency of rare exonic deletions that overlap with PD associated genes in a pediatric ASD group. Three hundred and five children diagnosed with ASD were enrolled in a study focused on deep phenotyping and genomic profiling by chromosomal microarrays. In the investigated group, four children with ASD harbored deletions encompassing genes involved in Mendelian forms of PD or contributing to PD risk. Deletions of Parkin RBR E3 ubiquitin protein ligase ( PRKN) and synuclein alpha interacting protein ( SNCAIP ) were found in one patient, each; two other patients showed intragenic deletions of Rab9 effector protein with kelch motifs ( RABEPK ). Our study found that deletions involving genes associated with PD are rare events, as we identified approximately 1% in the ASD cohort of children. Our data adds to the previous reports of rare genomic imbalances of PD associated genes in ASD, further supporting the hypothesis that these conditions might share molecular mechanisms of pathogenesis.

Bladder cancer (BC) is the most frequent cancer of the urinary system and one of the most common malignancies in the world. In the last decade, many studies have been conducted to better understand the pathophysiological mechanisms of BC to find innovative markers for disease monitoring and treatment. In this study, we aim to identify miRNAs whose expression is associated with specific tumoral characteristics and risks of disease progression. Forty-one BC patients were enrolled in this study. The expression of 84 miRNAs was evaluated by qRT-PCR analysis on tumoral and peritumoral tissues. The results highlighted the association of the miRNA-17-92 cluster with BC, with miR-17-5p, miR-18a-5p, miR-19a-3p, and miR-20a-5p (members of this cluster) being upregulated in the tumoral tissue and correlated with muscle invasion and tumor grading. Taken together, our study identified a panel of 26 dysregulated miRNAs in BC, some of which may be associated with aggressiveness and the risk of progression of this malignancy.

Despite recent advances in targeted cancer therapies, drug resistance remains an important setback in tumor control. Understanding the complex mechanisms involved in both innate and acquired drug resistance represents the first step in discovering novel therapeutic agents. Because of its importance in tumorigenesis, progression, and metastasis, lipid metabolism is increasingly garnering attention. CD36 is a membrane receptor at the top of the signaling cascade that transports lipids. Its expression has been repeatedly presented as an unfavorable prognostic factor for various tumor types, raising the question: could CD36 be a critical factor in cancer treatment resistance? In our review, we set out to explore the most prominent studies on the implication of CD36 in resistance to platinum-based drugs and other adjuvant cancer therapies in solid and haematological neoplasia. Moreover, we provide an overview of the latest anti-CD36 cancer therapies, thus opening new perspectives for future personalized medicine.

For more than 40 years, autologous platelet concentrates have been used in clinical medicine. Since the first formula used, namely platelet-rich plasma (PRP), other platelet concentrates have been experimented with, including platelet-rich fibrin and concentrated growth factor. Platelet concentrates have three standard characteristics: they act as scaffolds, they serve as a source of growth factors and cytokines, and they contain live cells. PRP has become extensively used in regenerative medicine for the successful treatment of a variety of clinical (non-)dermatological conditions like alopecies, acne scars, skin burns, skin ulcers, muscle, cartilage, and bone repair, and as an adjuvant in post-surgery wound healing, with obvious benefits in terms of functionality and aesthetic recovery of affected tissues/organs. These indications were well documented, and a large amount of evidence has already been published supporting the efficacy of this method. The primordial principle behind minimally invasive PRP treatments is the usage of the patient’s own platelets. The benefits of the autologous transplantation of thrombocytes are significant, representing a fast and economic method that requires only basic equipment and training, and it is biocompatible, thus being a low risk for the patient (infection and immunological reactions can be virtually disregarded). Usually, the structural benefits of applying PRP are attributed to fibroblasts only, as they are considered the most numerous cell population within the interstitium. However, this apparent simplistic explanation is still eluding those different types of interstitial cells (distinct from fibroblasts) that are residing within stromal tissue, e.g., telocytes (TCs). Moreover, dermal TCs have an already documented potential in angiogenesis (extra-cutaneous, but also within skin), and their implication in skin recovery in a few dermatological conditions was attested and described ultrastructurally and immunophenotypically. Interestingly, PRP biochemically consists of a series of growth factors, cytokines, and other molecules, to which TCs have also proven to have a positive expression. Thus, it is attractive to hypothesize and to document any tissular collaboration between cutaneous administered PRP and local dermal TCs in skin recovery/repair/regeneration. Therefore, TCs could be perceived as the missing link necessary to provide a solid explanation of the good results achieved by administering PRP in skin-repairing processes.

Psychotic disorders are a heterogenous class of mental illness, with an intricate pathophysiology, involving genetics and environmental factors, and their interaction. The identification of accessible biomarkers in bodily systems such as blood may lead to more accurate diagnosis, and more effective treatments targeting dysfunctional pathways, and could assist in monitoring the disease evolution. This systematic review aims to highlight the dysregulated microRNAs (miRNAs) in the peripheral blood of patients with psychotic disorders. Using the PRISMA protocol, PubMed and Science Direct databases were investigated and 22 articles were included. Fifty-five different miRNAs were found differentially expressed in the blood of psychotic patients compared to controls. Seventeen miRNAs (miR-34a, miR-181b, miR-432, miR-30e, miR-21, miR-137, miR-134, miR-7, miR-92a, miR-1273d, miR-1303, miR-3064-5p, miR-3131, miR-3687, miR-4428, miR-4725-3p, and miR-5096) were dysregulated with the same trend (up- or down-regulation) in at least two studies. Of note, miR-34a and miR-181b were up-regulated in the blood of psychotic patients in seven and six studies, respectively. Moreover, the level of miR-181b in plasma was found to be positively correlated with the amelioration of negative symptoms. The panel of miRNAs identified in this review could be validated in future studies in large and well-characterized cohorts of psychotic patients.

Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive and lethal forms of cancer. The symptoms appear in advanced stages, and diagnostic and prognostic tests for the early detection of PDAC and disease evolution are not available. The dysregulation of microRNAs (miRNAs) has been associated with cancer development and progression, and some miRNAs have been reported to promote specific metastasis. In this study we aimed to identify the miRNAs dysregulated in PDAC tumoral tissues and a subset of miRNAs associated with tumoral characteristics, mainly metastasis presence and site. For this, the expression of 84 miRNAs was evaluated by qPCR in 30 tumoral tissues and 16 samples of non-tumoral pancreatic tissues. The comparison revealed 32 dysregulated miRNAs (19 upregulated and 13 downregulated) in the PDAC group. Reactome pathway over-representation analysis revealed that these miRNAs are involved in several biological pathways, including "ESR-mediated signaling", "PIP3 activates AKT signaling", and "Regulation of PTEN", among others. Moreover, our study identified an upregulation of miR-15b-5p and miR-20b-5p in the tumoral tissues of patients with hepatic metastasis, outlining these miRNAs as potential markers for hepatic metastasis. No significant difference in miRNA expression was observed in relation to anatomic location, lymphovascular invasion, lung metastasis, and the presence of diabetes.

CD36, a fatty acid translocator and NRF2, a transcription factor, are two important players in inflammation and oxidative stress, including in the central nervous system. Both were associated with neurodegeneration as tilting arms of a balance: while activation of CD36 participates in neuroinflammation, activation of NRF2 seems to protect against oxidative stress and neuroinflammation. This study aimed to establish whether tilting the balance one way or the other, by knocking out either of them (NRF2-/- or CD36-/-), would show that one holds higher weight over the other in the cognitive behaviour of mice. We tested both young and old knockout animals in a long-term testing protocol (over one month), using the 8-arm radial maze,. Young NRF2-/- mice exhibited a sustained anxious-like behaviour, which was not recapitulated in old mice nor CD36 -/- mice of either age. Neither knockout strain exhibited cognitive alterations, although CD36 -/- mice showed some improvement over WT littermates. In conclusion, NRF2-/- seems to affect behaviour of mice early in life, and could be considered a vulnerability factor for neurocognition, while CD36 impact on cognitive protection of the aging brain requires more investigation.

Fifteen years after their discovery, telocytes (TCs) are yet perceived as a new stromal cell type. Their presence was initially documented peri-digestively, and gradually throughout the interstitia of many (non-)cavitary mammalian, human, and avian organs, including skin. Each time, TCs proved to be involved in diverse spatial relations with elements of interstitial (ultra)structure (blood vessels, nerves, immune cells, etc.). To date, transmission electron microscopy (TEM) remained the single main microscopic technique able to correctly and certainly attest TCs by their well-acknowledged (ultra)structure. In skin, dermal TCs reiterate almost all (ultra)structural features ascribed to TCs in other locations, with apparent direct implications in skin physiology and/or pathology. TCs' uneven distribution within skin, mainly located in stem cell niches, suggests involvement in either skin homeostasis or dermatological pathologies. On the other hand, different skin diseases involve different patterns of disruption of TCs' structure and ultrastructure. TCs' cellular cooperation with other interstitial elements, their immunological profile, and their changes during remission of diseases suggest their role(s) in tissue regeneration/repair processes. Thus, expanding the knowledge on dermal TCs could offer new insights into the natural skin capacity of self-repairing. Moreover, it would become attractive to consider that augmenting dermal TCs' presence/density could become an attractive therapeutic alternative for treating various skin defects.

COVID-19 mRNA vaccines effectively reduce incidence of severe disease, hospitalisation and death. The biodistribution and pharmacokinetics of the mRNA-containing lipid nanoparticles (LNPs) in these vaccines are unknown in humans. In this study, we used qPCR to track circulating mRNA in blood at different time-points after BNT162b2 vaccination in a small cohort of healthy individuals. We found that vaccine-associated synthetic mRNA persists in systemic circulation for at least 2 weeks. Furthermore, we used transmission electron microscopy (TEM) to investigate SARS-CoV-2 spike protein expression in human leukemic cells and in primary mononuclear blood cells treated in vitro with the BNT162b2 vaccine. TEM revealed morphological changes suggestive of LNP uptake, but only a small fraction of K562 leukemic cells presented spike-like structures at the cell surface, suggesting reduced levels of expression for these specific phenotypes.

The reprogramming of lipid metabolism has been highlighted in colorectal cancer (CRC) studies, suggesting a critical role for the scavenger receptor CD36 and fatty acid synthase (FASN) in this malignancy. In this study, we analyzed the gene expression levels of CD36, FASN, the cell surface glypican 4 (GPC4), and the two transporters SLC27A3 and SLC27A4 in 39 paired tumoral and peritumoral tissues from patients with CRC compared with 18 normal colonic mucosae. Moreover, the levels of seven miRNAs targeting CD36 and most of the analyzed genes were evaluated. We found a significant impairment of the expression of all the analyzed genes except GPC4 as well as the differential expression of miR-16-5p, miR-26b-5p, miR-107, miR-195-5p, and miR-27a-3p in the colonic mucosa of CRC patients. Interestingly, CD36 and miR-27a-3p were downregulated and upregulated, respectively, in tumoral tissues compared to peritumoral and control tissues, with a significant negative correlation in the group of patients developing lymph node metastasis. Our results sustain the relationship between CRC and fatty acid metabolism and emphasize the importance of related miRNAs in developing new therapeutic strategies.

In aged muscle, satellite cells’ symmetric and asymmetric divisions are impaired, and intrinsic and extrinsic complex mechanisms govern these processes. This review presents many updated aspects regarding muscle stem cells’ fate in normal and aging conditions. The balance between self-renewal and commitment divisions contributes to muscle regeneration, muscle homeostasis, aging, and disease. Stimulating muscle regeneration in aging could be a therapeutic target, but there is still a need to understand the many mechanisms that influence each other in satellite cells and their niche. We highlight here the general outlines regarding satellite cell divisions, the primary markers present in muscle stem cells, the aging aspects concerning signaling pathways involved in symmetric/asymmetric divisions, the regenerative capacity of satellite cells and their niche alteration in senescent muscle, genetics and epigenetics mechanisms implied in satellite cells aging and exercise effect on muscle regeneration in the elderly.