For a long time there have been claims that taking astragalus root lengthens telomeres. I have read some studies that profiled the ability of high-priced purportedly life-extending supplements such as purified cycloastrogenol, which is derived from astragalus, to produce significant effects.

Specifically:

http://www.ncbi.nlm.nih.gov/pubmed/21426483

Of note, TA-65 did not altered significantly the levels of targets of the Wnt (CD44, CyclinD1) or TGFβ (Fibronectin, Klf4 or p16) pathways (Sup Fig 4), further supporting that TA-65-dependent telomerase activation occurs through transcription factors regulated by the MAPK pathway, which may directly or indirectly regulate the mTERT promoter (hypothetical mechanism in Fig. 2h, based in our current findings and previous results (Wang et al. 1998; Greenberg et al. 1999; Chang & Karin 2001; Inui et al. 2001; Takakura et al. 2005; Pericuesta et al. 2006)).

Unfortunately MAPK is kind of a difficult pathway to activate. According to Wikipedia:

http://en.wikipedia.org/wiki/Mitogen-activated_protein_kinase

As mentioned above, MAPKs typically form multi-tiered pathways, receiving input several levels above the actual MAP kinase. In contrast to the relatively simple, phosphorylation-dependent activation mechanism of MAPKs and MAP2Ks, MAP3Ks have stunningly complex regulation. Many of the better-known MAP3Ks, such as c-Raf, MEKK4 or MLK3 require multiple steps for their activation. These are typically allosterically-controlled enzymes, tighly locked into an inactive state by multiple mechanisms.

I can’t imagine a simple herbal compound would be able to push all the right molecular biological buttons to activate this pathway so instead I took a look at other means of activation.

As is typical, the cancer researchers , with their brute force investigation of every possible way to kill a cancer cell through every conceivable pathway, have stumbled onto a possible mechanism of action for astragalus, though they don’t realize it, since their objective is to try to find ways to kill cancer cells that want to live forever and not make people and their healthy cells live forever.

http://www.ncbi.nlm.nih.gov/pubmed/19526459

AKT inhibits MAD1-mediated target genes (hTERT and ODC) transcription repression and promotes cell cycle and cell growth. However, mutated S145A MAD1 abrogates the inhibition by AKT. Thus, our results suggest that phosphorylation of MAD1 by AKT inhibits MAD1-mediated transcription suppression and subsequently activates the transcription of MAD1 target genes.

And then the cardiology people looking for ways to improve heart health have stumbled upon astragalus’s impact on heart health in the presence of toxins and how it regulates AKT:

http://www.ncbi.nlm.nih.gov/pubmed/25386226

. In addition, there was profound inhibition of p38MAPK and activation of Akt after APS treatment. These results demonstrate that [astragalus polysaccharide] APS could suppress oxidative stress and apoptosis, ameliorating doxorubicin-mediated cardiotoxicity by regulating the PI3k/Akt and p38MAPK pathways

So.. The idea here is that astragalus activates Akt which then inhibits MAD1 which then promotes hTERT which lengthens telomeres.