This 2019 Mexican review stated:

“We describe some of the molecular and physical characteristics of SFN, its mechanisms of action, and the effects that SFN treatment induces in order to discuss its relevance as a ‘miraculous’ drug to prevent aging and neurodegeneration. SFN has been shown to modulate several cellular pathways in order to activate diverse protective responses, which might allow avoiding cancer and neurodegeneration as well as improving cellular lifespan and health span.

NF-κB is in charge of inflammatory response regulation. Under basal conditions, NF-κB is sequestrated into the cytosol by IκB, but when pro-inflammatory ligands bind to its receptors, the IKK protein family phosphorylates IκB to degrade it via proteasome, so NF-κB is able to translocate into the nucleus and transcript several inflammatory mediators. Sulforaphane is capable to inhibit IκB phosphorylation and NF-κB nuclear translocation.

SFN upregulated Nrf2 expression by reducing DNA demethylation levels of the Nrf2 promoter. In another model using the triple-transgenic mouse model of Alzheimer’s disease (3 × Tg-AD), the use of SFN regulates the expression of the Brain-derived neurotrophic factor (BDNF) via HDAC inhibition, thus increasing H3 and H4 acetylation on the BDNF promoter. Enhancing BDNF expression as an effect of SFN treatment increased the neuronal content of several synaptic molecules like MAP 2, synaptophysin, and PSD-95 in primary cortical neurons of 3 × Tg-AD.”

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6885086/ “Sulforaphane – role in aging and neurodegeneration”

I came across this review while searching PubMed for sulforaphane commonalities with presentation topics in Part 2 of Reversal of aging and immunosenescent trends with sulforaphane. The review outlined some aging aspects and presented relevant sulforaphane studies. Others such as eye and muscle decline weren’t addressed.

Since sulforaphane’s “a ‘miraculous’ drug” in the Abstract, I expected but didn’t see corresponding excitement in the review body. Just phrases like “it is known” and non-specific “more research is needed.”

Other papers published after this review were found by a PubMed “sulforaphane signal aging” search:

• Inflammation and Premature Ageing in Chronic Kidney Disease
  

  “Persistent inflammation, premature ageing, and CKD share common regulatory patterns of distinct biological pathways. For instance, the transcription factor nuclear factor erythroid 2-related factor 2 (NRF2) is downregulated in all three conditions. NRF2 is currently a promising and the clinically most advanced signaling pathway for the treatment of both inflammation and premature ageing in CKD.”

• Potential Protective and Therapeutic Roles of the Nrf2 Pathway in Ocular Diseases: An Update
  

  “The use of Nrf2 activators (such as SFN pretreatment) or the overexpression of Nrf2 can reduce DNA fracture; upregulate Nrf2, NQO1, HO-1, etc.; and protect LECs from OS damage.”

• TGF-β in Hepatic Stellate Cell Activation and Liver Fibrogenesis-Updated 2019
  

  “The Nrf2 pathway to some extent protects the liver against toxin-induced fibrosis. An association between TGF-β, ROS, and Nrf2 was reported for the fibrogenic processes of several organs, including the liver. Sulforaphane, an Nrf2 activator, inhibited TGF-β signaling and reduced hepatic fibrosis in the BDL model.”

• Exercise-Induced Mitohormesis for the Maintenance of Skeletal Muscle and Healthspan Extension
  

  “Nrf2 activators may improve skeletal muscle quality and help maintain muscle function with age. Other Nrf2 activators, such as sulforaphane, demonstrate similar results, including improved mitochondrial and skeletal muscle function.”

• The Anti-Inflammatory and Anti-Oxidant Mechanisms of the Keap1/Nrf2/ARE Signaling Pathway in Chronic Diseases
  

  “The Nrf2 activator sulforaphane enhances running capacity in rats by upregulating Nrf2 signaling and downstream genes and attenuates muscle fatigue via reduction of oxidative stress caused by exhaustive exercise. Studies of Nrf2 activation as a response to resistance training produced less defined results. Mitochondrial ROS signaling repairs exercise-injured myofibers. Nrf2 activity was reported to reduce muscle glycogen content with resultant improved glucose tolerance.”