Life is indeed continuously going through the irreversible and inevitable process of aging. The rate of aging process depends on various factors and varies individually. These factors include various environmental stimuli including exposure to toxic chemicals, psychological stress whereas suffering with various illnesses specially the chronic diseases serve as endogenous triggers. The basic underlying mechanism for all kinds of stresses is now known to be manifested as production of excessive ROS, exhaustion of ROS neutralizing antioxidant enzymes and proteins leading to imbalance in oxidation and antioxidant processes with subsequent oxidative stress induced inflammation affecting the cells, tissues, organs and the whole body. All these factors lead to conventional cell death either through necrosis, apoptosis, or autophagy. Currently, a newly identified mechanism of iron dependent regulated cell death called ferroptosis, is of special interest for its implication in pathogenesis of various diseases such as cardiovascular disease, neurological disorders, cancers, and various other age-related disorders (ARD). In ferroptosis, the cell death occur neither by conventional apoptosis, necrosis nor by autophagy, rather dysregulated iron in the cell mediates excessive lipid peroxidation of accumulated lethal lipids. It is not surprising to assume its role in aging as previous research have identified some solid cues on the subject. In this review, we will highlight the factual evidences to support the possible role and implication of ferroptosis in aging in order to declare the need to identify and explore the interventions to prevent excessive ferroptosis leading to accelerated aging and associated liabilities of aging.

Colonization and development of the gut microbiome is a crucial consideration for optimizing the health and performance of livestock animals. This is mainly attributed to the fact that dietary and management practices greatly influence the gut microbiota, subsequently leading to changes in nutrient utilization and immune response. A favorable microbiome can be implanted through dietary or management interventions of livestock animals, especially during early life. In this review, we explore all the possible factors (for example gestation, colostrum, and milk feeding, drinking water, starter feed, inoculation from healthy animals, prebiotics/probiotics, weaning time, essential oil and transgenesis), which can influence rumen microbiome colonization and development. We discuss the advantages and disadvantages of potential strategies used to manipulate gut development and microbial colonization to improve the production and health of newborn calves at an early age when they are most susceptible to enteric disease. Moreover, we provide insights into possible interventions and their potential effects on rumen development and microbiota establishment. Prospects of latest techniques like transgenesis and host genetics have also been discussed regarding their potential role in modulation of rumen microbiome and subsequent effects on gut development and performance in neonatal ruminants.

• Gut microbial diversity dysbiosis leads to increased death in COVID-19. • High death tool in COVID-19 is due to microbiome disturbance in co-morbid patients. • More deaths in ICU Individual seems to be because of microbiome dysbiosis. • Probiotics can be a Supplementary Therapy to decrease death tool in COVID-19.

Purpose of Review: Atherosclerosis is the principal cause of cardiovascular diseases (CVDs) which are the major cause of death worldwide. Mechanical force plays an essential role in cardiovascular health and disease. To bring the awareness of mechanosensitive Piezo1 role in atherosclerosis and its therapeutic potentials we review recent literature to highlight its involvement in various mechanisms of the disease.

It is increasingly aware that gut microbiota is closely associated with atherosclerosis. However, which and how specific gut bacteria regulate the progression of atherosclerosis is still poorly understood. In this study, modified linear discriminant analysis was performed in comparing the gut microbiota structures of atherosclerotic and non-atherosclerotic mice, and Desulfovibrio desulfuricans (D. desulfuricans) was found to be associated with atherosclerosis. D. desulfuricans-treated Apoe^−/− mice showed significantly aggravated atherosclerosis. The proatherogenic effect of D. desulfuricans was attributed to its ability to increase intestinal permeability and subsequent raise in the transit of lipopolysaccharide (LPS) from the intestine to the bloodstream. Excessive LPS in the blood can elicit local and systemic inflammation and activate Toll-like receptor 4 (TLR4)/nuclear factor-κB (NF-κB) signaling of endothelial cells. TAK-242, a specific inhibitor of TLR4, can ameliorate the development of D. desulfuricans-induced atherosclerosis by blocking the LPS-induced activation of TLR4/NF-κB signaling.