Back

Statins and genetic inhibition of the mevalonate pathway activate an ATF3-STMN2 regenerative program

Nolan, M.; Aryal, S.; Ndayambaje, I. S.; Cao, M.; Lee, P.; Hovde, M.; Yun, S.; Wlaschin, J.; Held, A.; Beaussant, H.; Wymann, B.; Lee, C.-Z.; Lim, S. M.; Jiang, X.; Ramesh, N.; Agra Almeida Quadros, A. R.; Boulos, A.; Zinter, N.; Salem, S.; El-Tayar, L.; Beccari, M.; Presa, M.; Jourdan Ferraras Reyes, C.; Ruan, Y. Y.; Griesman, G.; Aguilar, C.; Hawrot, J.; Wheeler, H.; Melamed, Z.; P. Kleinstiver, B.; Albers, M.; W. Cleveland, D.; E. Tanzi, R.; M. Lutz, C.; D. Hubbard, R.; Kobayashi, D.; Ward, M.; R.R. Alves, C.; Wainger, B.; Le Pichon, C.; Lagier-Tourenne, C.

2026-02-24 neuroscience
10.64898/2026.02.23.707492 bioRxiv
Show abstract

Loss of neuronal regenerative capacity is a common feature of neurodegenerative disease and axonal injury, yet the transcriptional programs governing this state remain poorly defined. Stathmin-2 (STMN2), a tubulin-binding protein essential for axon maintenance and repair, is profoundly depleted following loss of nuclear TDP-43 in neurodegenerative disease. Here, we identify statins as potent inducers of STMN2 expression. Pharmacological and genetic suppression of the mevalonate pathway, and subsequent prevention of protein geranylgeranylation, restored STMN2 levels in TDP-43 deficient cells and promoted neurite growth. STMN2 induction was abrogated when using a statin analogue unable to interact with HMG-CoA reductase, and through co-administration of mevalonate or geranylgeranyl diphosphate substrates. RNA-seq revealed that statins induce a coordinated pro-regenerative transcriptional response, including activation of the AP-1 transcription factor complex gene, ATF3. Loss of ATF3 attenuated STMN2 induction in vitro, and diminished injury-induced Stmn2 upregulation in spinal motor neurons in vivo. These results demonstrate statins as modulators of ATF3 and STMN2 expression and highlight their therapeutic potential in neurodegenerative disease.

Matching journals

The top 7 journals account for 50% of the predicted probability mass.

1
Nature Communications
4913 papers in training set
Top 11%
14.2%
2
Journal of Clinical Investigation
164 papers in training set
Top 0.1%
10.0%
3
Cell Reports
1338 papers in training set
Top 3%
10.0%
4
EMBO Molecular Medicine
85 papers in training set
Top 0.1%
7.1%
5
Molecular Therapy
71 papers in training set
Top 0.7%
3.6%
6
Nature Neuroscience
216 papers in training set
Top 3%
3.0%
7
Molecular Neurodegeneration
49 papers in training set
Top 0.3%
2.7%
50% of probability mass above
8
Developmental Cell
168 papers in training set
Top 6%
2.7%
9
Acta Neuropathologica
51 papers in training set
Top 0.4%
2.3%
10
Cell Death & Disease
126 papers in training set
Top 0.8%
1.9%
11
Aging Cell
144 papers in training set
Top 2%
1.9%
12
Science Advances
1098 papers in training set
Top 18%
1.7%
13
Brain
154 papers in training set
Top 3%
1.7%
14
Cell Reports Medicine
140 papers in training set
Top 4%
1.6%
15
Nature Metabolism
56 papers in training set
Top 1%
1.6%
16
Proceedings of the National Academy of Sciences
2130 papers in training set
Top 36%
1.3%
17
JCI Insight
241 papers in training set
Top 4%
1.3%
18
The EMBO Journal
267 papers in training set
Top 3%
1.3%
19
Cell Chemical Biology
81 papers in training set
Top 2%
1.2%
20
Experimental Neurology
57 papers in training set
Top 0.9%
1.1%
21
Acta Neuropathologica Communications
81 papers in training set
Top 0.9%
0.9%
22
Neuron
282 papers in training set
Top 7%
0.9%
23
eLife
5422 papers in training set
Top 54%
0.9%
24
Science Translational Medicine
111 papers in training set
Top 5%
0.9%
25
Immunity
58 papers in training set
Top 4%
0.9%
26
Redox Biology
64 papers in training set
Top 0.7%
0.9%
27
PLOS Biology
408 papers in training set
Top 18%
0.8%
28
Journal of Neuroinflammation
50 papers in training set
Top 0.8%
0.8%
29
Neurobiology of Disease
134 papers in training set
Top 4%
0.7%
30
EMBO reports
136 papers in training set
Top 6%
0.7%