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4.4 Challenges and Prospectives 71
ssDNA
TDN-G-TPP
A
TA P
A
TA
KR
Aptamer
ssDNA
TPP
C C + N
–
N
+
P
+
N
V1 V2
V3 V4
Antisense
(a) (b)
Cytoplasm
Mitochondrion
Gene therapy
Nucleus
PDT
560 nm
ROS
Lysosome
Triphenyl phosphonium (TPP)
DNA aggregates
Targeting
G-quadruplex
DNA aggregates
coated mitochondria
Aerobic
respiration
Glycolysis
ADP-actin ATP-actin
Lamellipodium
T
Cell migration
ATP ADP
140 mM K
+
5 mM K
+
P
+
Figure 4.4 (a) The design of tetrahedral framework nucleic acids loading with functional nucleic
acid and protein. Source: Reproduced with permission Wu et al. [106]. Copyright 2020, American
Chemical Society. (b) The form of dynamic aggregates with tetrahedral framework nucleic acids on
mitochondrial membrane. Source: Reproduced with permission Li et al. [107]. Copyright 2022,
American Chemical Society.
4.4 Challenges and Prospectives
In summer, whether it is a simple nucleic acid therapeutic drug or the development of a
framework nucleic acid-based delivery system, it provides a guiding inquiry into the treat-
ment of mitochondrial dysfunction, although most studies are still stayed in vitro. Due to the
limited knowledge of the mechanism of action of nucleic acids entering the mitochondria,
there is a clear obstacle to the optimization of nucleic acid structure.
https://t.me/med1917
72 4 The Application of Framework Nucleic Acid-Based Nanomaterials
Traditional drug delivery systems exhibit poor permeability when passing through bio-
logical intrinsic barriers such as the blood–brain barrier and the blood–placental barrier
due to their size and structure, resulting in low eciency in drug treatment of serious dis-
eases, particularly central nervous system diseases. Mitochondrial dysfunction is linked to
a number of neurodegenerative disorders. Framework nucleic acid nanoparticles are eec-
tive in transmitting physiologicalbarriers. Taking the tetrahedral framework nucleic acid as
an example, its ability to cross the blood–brain barrier and transport drugs into nerve cells
[109, 110], combined with the neuroprotective eect and editable targeting of the tetrahe-
dral framework nucleic acid itself, will be expected to make it an ecient delivery system
for neuropathy caused by mitochondrial dysfunction [111, 112].
On the other hand, framework nucleic acid-based delivery systems have made a lot of
evidence in targeting cells, including in vivo and in vitro work, but they seem to be less pow-
erful in the study of targeted organelles; the number of studies in this area is small, and the
mechanism is not clearly elaborated. At present, the treatment of mitochondrial dysfunc-
tion diseases is mostly focused on cancer-related exploration, and there are fewer studies on
other dysfunctions such as calcium ion overload and abnormal mitochondrial dynamics.
Framework nucleic acids are a very promising delivery system that targets mitochondria
and may also have certain mitochondrial function regulation eects, such as tetrahedral
framework nucleic acids that regulate oxidative stress of cells. However, the specic mech-
anism by which framework nucleic acids carry small-molecule drugs or nucleic acids into
the mitochondria through two layers of mitochondrial membranes is unclear, which is also
a major limitation of the use of framework nucleic acids in the treatment of mitochon-
drial dysfunction. Secondly, the special structure of mitochondria is more conducive to the
targeting of positively charged and lipophilic materials [113], which is contrary to the nega-
tive electrical characteristics of the nucleic acids, and for the framework nucleic acid-based
delivery systems that wish to enter the mitochondria, it may be necessary to nd a more
systematic modication method to improve the targeting and entry eciency of the mito-
chondria.
In conclusion, the corrective role of nucleic acids in mitochondrial dysfunction is unlim-
ited, especially for the framework nucleic acid-based delivery systems. It is hoped that by
optimizing the structure and delivery mode of this delivery system, it can be applied more
accurately and eciently to cancer, neurodegenerative changes, genetic-related diseases,
and other diseases related to mitochondria.
Funding
This study was supported by the National Natural Science Foundation of China (81800947),
Sichuan Science and Technology Program (Grant 2020YFS0176), and the Postdoctoral Sci-
ence Foundation of China (Grants 2018M640930 and 2020T130443).
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