Obesity and osteoporosis are two alarming health disorders prominent among middle and old age populations, and the numbers of those affected by these two disorders are increasing. It is estimated that more than 600 million adults are obese and over 200 million people have osteoporosis worldwide. Interestingly, both of these abnormalities share some common features including a genetic predisposition, and a common origin: bone marrow mesenchymal stromal cells. Obesity is characterized by the expression of leptin, adiponectin, interleukin 6 (IL-6), interleukin 10 (IL-10), monocyte chemotactic protein-1 (MCP-1), tumor necrosis factor-alpha (TNF-α), macrophage colony stimulating factor (M-CSF), growth hormone (GH), parathyroid hormone (PTH), angiotensin II (Ang II), 5-hydroxy-tryptamine (5-HT), Advance glycation end products (AGE), and myostatin, which exert their effects by modulating the signaling pathways within bone and muscle. Chemical messengers (eg. TNF-α, IL-6, AGE, leptins) that are upregulated or downregulated as a result of obesity have been shown to act as negative regulators of osteoblasts, osteocytes and muscles, as well as positive regulators of osteoclasts. These additive effects of obesity ultimately increase the risk for osteoporosis and muscle atrophy. The aim of this review is to identify the potential cellular mechanisms through which obesity may facilitate osteoporosis, muscle atrophy and bone fractures.

Osteoporosis has become a serious health problem throughout the world which is associated with an increased risk of bone fractures and mortality among the people of middle to old ages. Diabetes is also a major health problem among the people of all age ranges and the sufferers due to this abnormality increasing day by day. The aim of this review is to summarize the possible mechanisms through which diabetes may induce osteoporosis. Diabetes mellitus generally exerts its effect on different parts of the body including bone cells specially the osteoblast and osteoclast, muscles, retina of the eyes, adipose tissue, endocrine system specially parathyroid hormone (PTH) and estrogen, cytokines, nervous system and digestive system. Diabetes negatively regulates osteoblast differentiation and function while positively regulates osteoclast differentiation and function through the regulation of different intermediate factors and thereby decreases bone formation while increases bone resorption. Some factors such as diabetic neuropathy, reactive oxygen species, Vitamin D, PTH have their effects on muscle cells. Diabetes decreases the muscle strength through regulating these factors in various ways and ultimately increases the risk of fall that may cause bone fractures.

Diabetic vascular diseases have emerged as a significant concern in medical research due to their considerable impact on human health. The challenge lies in the insufficient understanding of the intricate pathophysiological mechanisms associated with different forms of diabetic vascular diseases, which hampers our ability to identify effective treatment targets. Addressing this knowledge gap is essential for developing successful interventions. Unraveling the molecular pathways through which diabetes leads to microvascular and macrovascular complications in vital organs such as the heart, brain, kidneys, retina, and extremities is crucial. Notably, oxidative stress resulting from hyperglycemia is the key factor in initiating these complications. This review aims to elucidate the specific molecular mechanisms by which oxidative stress drives microvascular and macrovascular diseases and to highlight promising therapeutic advancements that offer hope for effective treatment solutions.

According to the World Health Organization, metabolic syndrome (MetS) can be defined as a pathological condition characterized by abdominal obesity, insulin resistance, hypertension, and hyperlipidemia. The incidence of MetS keeps rising, as at least 35% of the USA population suffers from MetS. One of the worst comorbidities of metabolic syndrome are cardiovascular diseases that significantly amplifies the mortality associated with this syndrome. There is an urgent need to understand the pathophysiology of MetS to find novel diagnosis, treatment and management to mitigate the MetS and associated complications. Altered circulatory adiponectin levels have been implicated in MetS. Adiponectin has numerous biologic functions including antioxidative, anti-nitrative, anti-inflammatory, and cardioprotective effects. Being a pleiotropic hormone of multiple tissues, tissue-specific key signaling pathways of adiponectin will help finding specific target/s to blunt the pathophysiology of metabolic syndrome and associated disorders. The purpose of this review is to elucidate tissue-specific signaling pathways of adiponectin and possibly identify potential therapeutic targets for MetS as well as to evaluate the potential of adiponectin as a biomarker/therapeutic option in MetS.

Over 30 million Americans are diagnosed with diabetes and this number is only expected to increase. There are various causes that induce complications with diabetes, including oxidative stress. In oxidative stress, lipid peroxidation-derived reactive carbonyl species such as 4-hydroxy-2-nonenal (4-HNE) is shown to cause damage in organs that leads to diabetic complications. We provided evidence to show that 4-HNE or/and 4-HNE-protein adducts are elevated in various organ systems of diabetic patients and animal models. We then discussed the advantages and disadvantages of different methodologies used for the detection of 4-HNE in diabetic tissues. We also discussed how novel approaches such as electrochemistry and nanotechnology can be used for monitoring 4-HNE levels in biological systems in real-time. Thus, this review enlightens the involvement of 4-HNE in the pathogenesis of diabetes and its complications and efficient methods to identify it. Furthermore, the article presents that 4-HNE can be developed as a biomarker for end-organ damage in diabetes such as diabetic cardiac complications.

Tumor angiogenesis, the formation of new blood vessels within the tumor microenvironment, is considered a hallmark of cancer progression and represents a crucial target for therapeutic intervention. The tumor microenvironment is characterized by a complex interplay between proangiogenic and antiangiogenic factors, regulating the vascularization necessary for tumor growth and metastasis. The study of angiogenesis involves a spectrum of techniques, spanning from biomarker assessment to advanced imaging modalities. This comprehensive review aims to provide insights into the molecular intricacies, regulatory dynamics, and clinical implications of tumor angiogenesis. By delving into these aspects, we gain a deeper understanding of the processes driving vascularization in tumors, paving the way for the development of novel and effective antiangiogenic therapies in the fight against cancer.