Microbiome interactions with different risk factors in development of myocardial infarction.

Among all non-communicable diseases, Cardiovascular Diseases (CVDs) stand as the leading global cause of mortality. Within this spectrum, Myocardial Infarction (MI) strikingly accounts for over 15 % of all deaths. The intricate web of risk factors for MI, comprising family history, tobacco use, oral health, hypertension, nutritional pattern, and microbial infections, is firmly influenced by the human gut and oral microbiota, their diversity, richness, and dysbiosis, along with their respective metabolites. Host genetic factors, especially allelic variations in signaling and inflammatory markers, greatly affect the progression or severity of the disease. Despite the established significance of the human microbiome-nutrient-metabolite interplay in associations with CVDs, the unexplored terrain of the gut-heart-oral axis has risen as a critical knowledge gap. Moreover, the pivotal role of the microbiome and the complex interplay with host genetics, compounded by age-related changes, emerges as an area of vital importance in the development of MI. In addition, a distinctive disease susceptibility and severity influenced by gender-based or ancestral differences, adds a crucial insights to the association with increased mortality. Here, we aimed to provide an overview on interactions of microbiome (oral and gut) with major risk factors (tobacco use, alcohol consumption, diet, hypertension host genetics, gender, and aging) in the development of MI and therapeutic regulation.

Catalytic resilience of multicomponent aromatic ring-hydroxylating dioxygenases in Pseudomonas for degradation of polycyclic aromatic hydrocarbons.

Hydrophobic organic compounds, either natural or introduced through anthropogenic activities, pose a serious threat to all spheres of life, including humankind. These hydrophobic compounds are recalcitrant and difficult to degrade by the microbial system; however, microbes have also evolved their metabolic and degradative potential. Pseudomonas species have been reported to have a multipotential role in the biodegradation of aromatic hydrocarbons through aromatic ring-hydroxylating dioxygenases (ARHDs). The structural complexity of different hydrophobic substrates and their chemically inert nature demands the explicit role of evolutionary conserved multicomponent enzyme ARHDs. These enzymes catalyze ring activation and subsequent oxidation by adding two molecular oxygen atoms onto the vicinal carbon of the aromatic nucleus. This critical metabolic step in the aerobic mode of degradation of polycyclic aromatic hydrocarbons (PAHs) catalyzed by ARHDs can also be explored through protein molecular docking studies. Protein data analysis enables an understanding of molecular processes and monitoring complex biodegradation reactions. This review summarizes the molecular characterization of five ARHDs from Pseudomonas species already reported for PAH degradation. Homology modeling for the amino acid sequences encoding the catalytic α-subunit of ARHDs and their docking analyses with PAHs suggested that the enzyme active sites show flexibility around the catalytic pocket for binding of low molecular weight (LMW) and high molecular weight (HMW) PAH substrates (naphthalene, phenanthrene, pyrene, benzo[α]pyrene). The alpha subunit harbours variable catalytic pockets and broader channels, allowing relaxed enzyme specificity toward PAHs. ARHD's ability to accommodate different LMW and HMW PAHs demonstrates its 'plasticity', meeting the catabolic demand of the PAH degraders.