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1. Introduction

Ribosome is the ribonucleoprotein particle, which is an organelle for protein synthesis in cells, and its function is to synthesize the polypeptide chain efficiently and accurately according to the information of mRNA. Ribosomes can be found in almost all cells and even the smallest and simplest mycoplasma cell contains hundreds of them. At present, only mammalian mature red blood cells have no ribosomes, therefore, ribosomes are an indispensable structure of most cells. Mitochondria and chloroplasts contain ribosomes that synthesize their own proteins, which may be related to the origin of mitochondria and chloroplasts. The accepted endosymbiotic origin theory holds that mitochondria and chloroplasts originated from symbiotic bacteria and cyanobacteria in primitive eukaryotic, respectively. Therefore, mitochondrial ribosomes are more similar to the bacterial ribosomes than to cytoplasmic ribosomes. Mitochondrial ribosomal proteins (MRPs) are encoded by nuclear genes and synthesized by the cytoplasm 80S ribosomes, after specific targeting, sorting, transporting to mitochondria, and then assembling into mitochondrial ribosome small and large subunits with two rRNAs encoded by mitochondrial DNA (mt-DNA).

2. MRPs Associated with Diseases

With the research on MRPs, their names have changed [1], as shown in Table 1. The table also shows the changes of MRPs in tumor tissues reported in the past 5 years.

Table 1. Summary of the relationship between abnormal expression of mitochondrial ribosomal proteins and their encoding genes with diseases in recent 5 years.

3. Conclusions and Perspectives

The development of a high-precision analysis technology of cryo-electron microscopy enables us to identify the structure of mitochondrial ribosomal proteins with a scale of 0.1 nm. Each of the 80 MRPs is essential for the mitochondrial ribosome composition, which plays an irreplaceable role in the assembly and translation of mitochondrial DNA. At present, studies of the relationship between MRPs and cell apoptosis are few. Although the apoptotic mechanisms of MRPS29, MRPL41 and MRPL65 have not been fully elucidated, they at least provide us with useful information to deeply study the apoptotic mechanisms of MRPs. We can further explore the changes of MRPs function or pathway-activating role in the process of inducing apoptosis, based on the analysis of the MRPs structure. Additionally, specific mechanisms can be clarified in the future.

The abnormal expression of MRPs and their encoding genes is closely associated with a variety of cancer and mitochondrial related diseases. Multiple MRPs are important predictors of disease diagnosis. However, the specific mechanisms of inducing the development of diseases is little known.

In the future, on the one hand, it is very important to strengthen the research on the relationship between the abnormal expression of MRPs, lack of their encoding genes, and diseases. On the other hand, some MRPs such as MRPS22, MRPL44 and MRPL28 that have been clarified as key factors in the development of cancer, which can be as biological targets to deeply study their specific pathways of influence, in order to lay a theoretical foundation for a targeted diagnosis and therapy of cancer in our research.

This entry is adapted from the peer-reviewed paper 10.3390/ijms21228879