| ABSTRACT |
The pathological process, which occurs in the restoration of blood flow to ischemic tissues, is called ischemia-reperfusion (I/R) injury and has a counterproductive outcome of the development of cellular and mitochondrial damage due to oxidative stress, calcium overload, and inflammation. The mitochondria are the major origin and destination of reactive oxygen species (ROS) in the process of I/R, and thus are important targets in therapeutic intervention to protect the cells. Pharmacological approaches to mitochondrial maintenance, such as the mitochondrial permeability transition pore (mPTP) regulation, mitochondrial biogenesis promotion, and mitochondrial maintenance of dynamic, have demonstrated potential usefulness in reducing the effect of I/R on tissue damage. Cyclosporin A, MitoQ, SkQ1, and SS-31 are some of the agents that inhibit mPTP opening, stabilize mitochondrial membranes, and inhibit apoptosis. Moreover, the activators of AMPK, SIRT1, PPARs, and Nrf2 stimulate the biogenesis of mitochondria through the peroxisome proliferator-activated receptor co-activator 1 (PGC-1) experiment, increasing energy metabolism and antioxidant defense. Inhibition of Drp1-mediated fission and stimulation of fusion protein synthesis, i.e. Mfn2 and OPA1, is a modification of mitochondrial dynamics that keep mitochondrial integrity and cell viability intact. Biogenesis and dynamics are in balance assuring high quality control of mitochondria during reperfusion. In summary, the activation of mitochondrial protection with a combination of pharmacological control of mPTP, biogenesis, and dynamics |
| AUTHOR |
Isha, Bhumi Ruhil, Shafkat Huusain malik, Imtiyaz Hussain
School of Pharmacy, Desh Bhagat University, Mandi Gobindgarh, Punjab, India |
