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. 2022 Apr 27;16:867034. doi: 10.3389/fnins.2022.867034

FIGURE 2.

FIGURE 2

Possible role of Gap Junction Channels (GJC) in the propagation of cisplatin-induced cellular signals. (1) Cisplatin (CDDP) can potentially enter supporting cells (SCs) through non-selective transporters such as OCT2. Inside the cells, cisplatin induces toxicity by damaging DNA and mitochondria, producing ROS and other death signals that can propagate through GJC, spreading cell death signals through the sensory epithelium (Bystander effect). (2) Cisplatin can potentially enter SCs that lack intercellular communication through gap junctions, which restrict toxicity only to these cells. (3) Alternatively, GJC can potentially allow the transmission of protective signals that can reduce cell death between the coupled cells affected by cisplatin. (4) The loss of gap junction communication induced by cisplatin could also induce loss of cell viability in SCs.