The emergence of Multi-Drug Resistance (MDR) in treating Tuberculosis
(TB) has been led by the unnecessary overconsumption of anti tubercular drugs. MDR
being a multifactorial phenomenon is governed by many unknown mechanisms, hence
dissecting novel mechanisms for combating MDR is urgently needed. The success of
pathogenic Mycobacterium tuberculosis (Mtb) as a dreadful pathogen is due to its
capability to persist in chronic infection, despite of the robust immune response by the
host. During the course of infection, Mtb resides inside the host macrophages which in
turn provide a relatively hostile environment to the pathogen. This host pathogen
interaction causes the macrophages to undergo maturation, leading to lowering of pH
and limiting nutrients, including magnesium (Mg2+). Since Mg2+ is the most abundant
divalent cation in living cells it is mandatory for all organisms to maintain its
physiological levels to an optimum concentration. Mg2+ has a critical role in stabilizing
membranes, ribosomes, required as a cofactor in various enzymatic reactions and the
neutralization of nucleic acids. Thus harnessing the Mg2+ dependent pathways in Mtb
could be targeted as effective anti-TB strategy. This chapter helps in gaining insights
into the association of Mg2+ in survival of Mtb and how it can be exploited as potential
anti-mycobacterial drug targets.
Keywords: Anti-TB target, Drug resistance, Magnesium, MgtC, Mycobacterium.Anti-TB target, Drug resistance, Magnesium, MgtC, Mycobacterium.
