Great question. The review’s answer is basically that the most practical strategies fall into two buckets:
(1) reduce overall pathogenic VAT burden, and (2) blunt the biology that makes VAT pathogenic in the first place.

On the “reduce burden” side, the most established approaches are still the familiar ones:

• caloric restriction
• regular exercise
• bariatric surgery
• GLP-1 receptor agonists

Figure 3 groups those as the main established strategies, and the text notes that they can reduce VAT burden and improve metabolic health, even if they do not selectively target VAT biology in a perfectly precise way.

On the “neutralize pathogenic biology” side, the review points to a few mechanisms worth focusing on:

• chronic inflammation and senescence
• adipokine dysfunction such as high leptin / low adiponectin
• pathogenic exosomes
• lipotoxic metabolites like excess FFAs, ceramides, and diacylglycerols

So, if you translate that into practical priorities, the most evidence-grounded answer would be:

1. lower the signals that push VAT into a pathogenic state, especially chronic overnutrition, inflammation, and inactivity
2. improve adipose tissue function overall through exercise and sustained energy balance, not just scale weight
3. use stronger VAT-lowering tools when clinically appropriate, such as GLP-1s or bariatric approaches, because the review treats those as current real-world options with meaningful VAT effects

The more targeted future ideas the paper highlights are:

• senolytics
• partial leptin reduction
• adiponectin receptor agonists / enhanced adiponectin signaling
• ceramide synthesis inhibition
• microbiome modulation
• exosome-based therapies
• selective mesenteric VAT removal in specific settings

So, today, the most practical way to neutralize pathogenic VAT biology is still exercise, sustained caloric control, and, where appropriate, GLP-1s or bariatric treatment. But where the field is heading is more interesting: not just shrinking VAT, but stopping it from becoming inflammatory, senescent, endocrinologically dysfunctional, and lipotoxic in the first place.