Bone marrow adipose tissue (BMAT) is increasingly recognized as a metabolically active, endocrine, and immunomodulatory component of the marrow niche rather than a passive fat depot. This narrative review synthesizes biological, imaging, epidemiological, and therapeutic evidence linking BMAT and marrow metabolic activation with cardiometabolic disease. BMAT arises from marrow stromal progenitors and exhibits depot-specific heterogeneity, endocrine activity, insulin responsiveness, and context-dependent expansion during aging, diabetes, obesity, menopause, osteoporosis, and chronic kidney disease. Mechanistically, experimental studies indicate that marrow adipocytes and adipocyte-lineage niche cells can influence hematopoiesis through metabolic and local signaling, whereas trained immunity is established primarily in HSPCs, myeloid progenitors, and monocyte/macrophage populations. Human MRI/MRS studies characterize BMAT quantity and composition, whereas [18]F-FDG PET reflects non-BMAT-specific marrow activation associated with vascular inflammation and early atherosclerosis; direct BMAT-cardiovascular evidence remains limited. Emerging population imaging and genetic analyses support BMAT as a disease-associated phenotype, particularly for osteoporosis and fractures. Interventions affecting metabolic, inflammatory, skeletal, or marrow pathways have differing degrees of BMAT-related evidence, and none has established that modifying BMAT improves cardiovascular outcomes. This review identifies BMAT as an emerging research phenotype while emphasizing that its causal, prognostic, and therapeutic relevance to cardiovascular disease remains unresolved.

Worldwide, thyroid cancer is 7th most prevalent cancer, with projections indicating further increases by 2035. Few studies indicate role of micro RNA and RAGE receptor in cancer development. We hypothesize that micro RNA 500 may be associated with thyroid cancer development by effecting the AGE-RAGE axis. For the first time this study reported that miRNA-500 expression was higher in serum of subjects with papillary thyroid carcinoma (PTC) as compared to healthy controls. Similarly, higher levels of Advanced glycation end Products (AGEs) were seen and positively associated with mi-RNA500, in serum of PTC patients. While comparing the cancer and normal tissue of PTC patients we found enhanced expression of miRNA-500, RAGE receptor gene and protein in cancer tissue. RAGE ligands including HMGB-1 and S-100 were also found elevated in PTC cancer tissue as compared to normal tissue. In human thyroid cancer cells overexpressing miRNA-500 showed enhanced NFkB expression and oxidative stress however, this effect was diminished after blocking RAGE, linking miRNA-500 and RAGE together in development of thyroid cancer. Protein-protein interaction (PPI) pathway analysis further suggested that miR-500 target genes are embedded within a broader inflammatory signaling framework relevant to thyroid cancer biology. Our results demonstrate the association of miRNA-500 with RAGE axis along with preliminary evidence of pharmacological modulation, in thyroid cancer.