THE MITOCHONDRIAL DISEASES

The process of targeting drugs to the mitochondria to get therapeutic gain lies in the fact

that the mitochondria plays a big role in energy metabolism regulation, apoptosis, and reactive

oxygen species (ROS) production. It implies that when specific drugs are introduced into the

mitochondria, they provide the foundation to cure various diseases. Examples of the therapeutic

applications are antioxidants to mitochondria which prevent oxidative damage, toxic drugs or the

Bcl-2 proteins to the mitochondria which trigger apoptosis in the cancer therapy. There is also

the introduction of drugs to the mitochondria that inhibits mitochondrial permeability transition

(MPT) used in IR-related injuries in the tissue, for instance in stroke and heart attack. Finally, the

introduction of drugs to uncouple electron transport chain (ETC), also activating the uncoupling

proteins (UCPs) in diabetes and obesity. Other various methods have been introduced to achieve

the specific targeting, for example, the use of the soluble polymer carrier processes, liposome-

based strategies, and micelles. At the level of the subcellular, potential drug targets are the

nucleus used for gene therapy, the mitochondria for the proapoptotic therapies in cancer and also

replacement enzyme therapies which are for the lysosomal storage diseases. An example is the

Gaucher disease which is a lipid storage disease and has been successfully treated through

replacement of lysosomal enzyme glucocerebrosidase, also proapoptotic Bcl-2 to induce the

apoptosis in the cancer therapy. Some other diseases with the mitochondrial component like

diabetes, IR tissue, and the neurodegenerative diseases shall offer the same chances in the

mitochondrial drug therapy. It is most possibly that they will get success.

Amid apoptosis, mitochondria are key organelles to detect and enhance harm,

discharging cytochrome c and different cofactors for the effector caspases that disassemble the

cell. This discharge, firmly controlled by proteins of the Bcl-2 family, is joined by fracture of the
mitochondrial arrange and renovating of the mitochondrial cristae. The two procedures are

required for the movement of apoptosis and cristae redesigning is downstream of discontinuity.

Amid cell life and passing, mitochondrial shape is directed by a developing group of master

splitting (the cytoplasmic dynamin-related protein 1, Drp1; and its mitochondrial receptor parting

1, Fis1) and ace combination (the expansive GTPases Optic Atrophy 1, Opa1, in the internal

layer and Mitofusin, Mfn, 1 and 2 in the external mitochondrial film) mitochondria-molding

proteins.

Neurons are very subject to mitochondria since they are described by high vitality

requests and can't change to glycolysis when mitochondrial oxidative phosphorylation is

impeded. Countless maladies are in reality caused by a debilitation of mitochondrial work. All

the more as of late, changes in the qualities coding for mitochondria-forming proteins have been

related to some hereditary neurodegenerative sicknesses, embroiling mitochondrial shape

direction in the soundness of neurons. What's more, significant intrigue was as of late caught by

the part of mitochondrial morphology changes in familial types of Parkinson's infection (PD)

caused by transformations in the PINK1 and PARKIN qualities, be it essential or amplificatory?

Regardless of whether mitochondrial morphology assumes a part likewise in Huntington's illness

(HD) stays to be clarified.