Bhatti, Gurjit KaurPahwa, ParasGupta, AnshikaSidhu, Inderpal SinghNavik, Uma ShankerReddy, P. HemachandraBhatti, Jasvinder Singh2024-01-212024-08-142024-01-212024-08-142022-09-289789811654220978981165421310.1007/978-981-16-5422-0_175http://10.2.3.109/handle/32116/4338Mitochondria are essential for the metabolism of energy, regulation of apoptosis, and cell signaling. Overproduction of reactive oxidation species (ROS) in mitochondria is one of the indications of cancer cells. Moreover, this boosts the proliferation of cancerous cells by causing genomic instability and altering gene expressions. Mitochondrial and nuclear DNA mutations caused by oxidative damage impair the mechanism of oxidative phosphorylation and can lead to more mitochondrial ROS output, genome instability, and cancer development. The classic approach to target mitochondria of cancerous cells with novel targeted therapeutics helps in targeting the mitochondrial apoptotic proteins and changing energy metabolism. A key benefit of selective drug delivery is that it reduces the drug�s toxicity and increases specificity. A better understanding of the mitochondrial role in tumor growth will help design more therapeutic agents with better selectivity. � Springer Nature Singapore Pte Ltd. 2022.en-USBioenergetic therapyCancerMitochondriaMitochondrial medicineROSTargeted drug deliveryBook chapterhttps://link.springer.com/10.1007/978-981-16-5422-0_175