Hello, I’m Dr. Hocheol Shin, or “Dr. Shin.” I study feline kidney health and aging at Greycoat Research.

I earned my Ph.D. studying cancer and immunology, and I’m now building on that experience to explore how we can help cats stay healthier for longer.

In “Reading Papers with Dr. Shin,” we’ll explore research related to feline health together. We’ll look a little deeper into how things work, what the studies actually found, and what those findings might mean for our cats. I’ll explain any unfamiliar terms as we go.

Ready to open today’s paper with Lulu?

< Three-Sentence Summary >

1. If resveratrol helps turn down inflammatory signaling, quercetin may add a second layer: supporting the clearance of old, damaged cells.

2. In a feline study using a quercetin-derived herbal compound, the inflammatory marker SAA decreased markedly in both healthy and obese cats.

3. The study was led by Dr. Arai and Dr. Kobayashi, scientific advisors to Greycoat Research, and quercetin is one of the ingredients Greycoat Research is evaluating and incorporating into its product design. 

< Introduction >

In the previous installment on resveratrol (RSV), we discussed how a compound found in grape skin can switch on the body’s “longevity machinery” and influence inflammation and aging.

Today’s subject, quercetin, is a close cousin of RSV. It is a flavonoid, which is a yellow plant pigment, found in everyday foods such as onions, apple skin, kale, and broccoli. And interestingly, it presses many of the same molecular switches as RSV.

But quercetin walks the RSV path and then extends one branch further. It is increasingly studied for its ability to clear away old, damaged cells – a property that is not unique to quercetin but is shared across this class of polyphenols, with quercetin being one of the better-studied members. We will cover that dimension as well.

One thing to flag upfront, exactly as with the RSV piece: the main feline study here is in obese cats, not cats with CKD. We discuss it because obesity and CKD are linked through chronic low-grade inflammation – and that is precisely the axis quercetin appears to act on. 

< Background >

If you read Part 1, you already know the core mechanism. RSV works largely by flipping a set of cellular switches: SIRT1, which is related to longevity and metabolism; NF-κB, a major inflammatory signaling pathway; and Nrf2, which supports antioxidant defense.

The one-line update for today is simple: quercetin appears to press many of the same switches. Same machinery, different compound. So I won’t re-explain the full pathway here. Part 1 has the longer version.

What earns quercetin its own article is a second mechanism that the RSV story did not focus on: clearing out aged cells. 

1. Senescent Cells – the “Zombie Cell” Problem

When a cell is too damaged, it normally bows out and removes itself. But some cells get stuck in between. They neither die nor function properly. They linger, take up space, and continuously release inflammatory signals into the tissue around them.

These are senescent cells, better known by their nickname: “zombie cells.”

Here’s why they matter. A zombie cell is not passive. It is a small, persistent source of inflammation. As these cells accumulate with age, they become one of the drivers of chronic low-grade inflammation, the kind of slow internal stress that is closely tied to organ aging and, of central interest to us, kidney decline.

The conventional approach is to suppress the inflammation they cause. The newer approach is more direct: remove the zombie cells themselves. 

2. Senolytics – Taking Out the Source

Compounds that selectively encourage senescent cells to finally self-destruct are called senolytics.

Quercetin is one of the most-studied senolytic candidates. That is the real reason it deserves a chapter of its own, not just a footnote to resveratrol. In the Supporting Evidence section, we will look at how this idea has been tested, including in a kidney-disease context. 

< Main Study: Quercetin Derivatives in Cats >

Kobayashi M et al. “Effects of Supplementation with Anti-Inflammatory Compound Extracted from Herbs in Healthy and Obese Cats. Vet Med (Auckl). 2020;11:39-44.

Study Design

Healthy cats and obese cats received a herbal extract whose principal active component was a quercetin derivative. It was given in capsule form at approximately 2.5–3.0 mg/kg/day, expressed as quercetin equivalent, for four weeks.

Researchers measured plasma metabolites, hormones, and enzyme activities before and after supplementation. These included serum amyloid A (SAA), total cholesterol (T-Cho), triglycerides (TG), non-esterified fatty acids (NEFA), adiponectin, and liver enzymes.
Key Results

• Healthy cats: SAA ↓ markedly (19.2 → 4.8 ng/mL); NEFA, MDA, and liver enzymes also decreased
  
  
• Obese cats: SAA ↓ sharply (194.3 → 27.6 ng/mL); T-Chol ↓ (200.3 → 167.3 mg/100 mL) and AST ↓ significantly
  
  
• Parameters showing no significant change:
  Bodyweight, BCS remained unchanged during the 4-week experimental period

This is the crucial point: quercetin did not make the cats lose weight. Instead, the changes were seen in inflammatory and metabolic markers. That is exactly the axis on which we have positioned SAA as an important marker in feline kidney-health research. 

Why This Matters

The finding that a quercetin-derived compound was associated with a marked reduction in SAA provides direct feline evidence that quercetin may engage the inflammaging axis.

Given the link between obesity, chronic low-grade inflammation, and renal stress, this carries meaningful relevance for how we think about long-term kidney health and supportive care in cats. The authors also noted that cats may respond to quercetin at a lower dose than dogs, with cats receiving 2.5–3.0 mg/kg/day compared with 5.0 mg/kg/day in dogs. This is an important feline-specific point. 

< Supporting Evidence: Mechanisms and Translation >

1. The SIRT1 Convergence

Cui Z et al. Therapeutic application of quercetin in aging-related diseases: SIRT1 as a potential mechanism. Front Immunol. 2022;13;943321.

This review paper summarizes how many of quercetin’s reported effects may run through SIRT1: activating Nrf2/HO-1 antioxidant defense, suppressing NF-κB and NLRP3 inflammatory signaling, and supporting mitochondrial function.

The key takeaway for this series is simple: the very switch RSV presses, quercetin appears to press too. When different compounds converge on the same pathway, it underscores how central that pathway may be and provides a rationale for studying them together. 

2. Quercetin in Humans – Clinical Evidence

Tabrizi R et al. The effects of quercetin supplementation on lipid profiles and inflammatory markers among patients with metabolic syndrome and related disorders: A systematic review and meta-analysis of randomized controlled trials. Crit Rev Food Sci Nutr. 2019;60(11):1855-1868.

A meta-analysis of 16 human randomized controlled trials found that quercetin significantly reduced total cholesterol, LDL cholesterol, and CRP, an inflammatory marker.

Notably, triglycerides did not change significantly in humans. In the obese cats, they decreased numerically, but the change was not statistically significant (p = 0.068). So cholesterol and inflammation appear to respond in a broadly similar direction across species, while some markers may vary depending on species, population, and study design. 

3. The Senolytic Dimension – Kidney Context

Hickson LJ et al. Senolytics decrease senescent cells in humans: preliminary report from a clinical trial of dasatinib plus quercetin in individuals with diabetic kidney disease. eBioMedicine. 2019;47:446-456.

A Mayo Clinic team administered a quercetin-containing senolytic combination to patients with diabetic kidney disease. Senescent-cell burden and systemic inflammation decreased, offering early human evidence that senescent-cell clearance is being explored in a kidney-disease population.

Importantly, quercetin was used here in combination with another agent, not alone. So this finding should be read as “research is moving in this direction in the kidney field,” rather than as evidence of a quercetin-only effect. 

< Limitations >

• No direct feline kidney-disease data currently exists for quercetin. The feline evidence comes from obese cats, over a short 4-week window, and used a quercetin derivative within a herbal complex rather than pure quercetin.
• The human evidence comes mainly from metabolic syndrome and related disorders, not cats.
•  The senolytic kidney finding was obtained with a combination of dasatinib and quercetin, not quercetin alone.
• In the senolytic study, senescent cells were measured mainly in fat and skin tissue rather than directly in kidney tissue.
• Whether the SAA reduction in cats reflects a direct anti-inflammatory action or is secondary to changes in metabolic or hepatic state cannot be resolved from the current data.
• Feline pharmacokinetic data for quercetin remain limited. 

< Personal Thoughts >

In the resveratrol piece, I noted that before a disease-modifying drug arrives, what we can realistically do is help keep the body’s internal environment as stable as possible.

Quercetin is best understood as a teammate playing alongside RSV. It shares the SIRT1 pathway, so the two may coordinate well from a mechanistic perspective. Quercetin also adds the senescent-cell angle on top.

What I find most compelling is that when quercetin was fed directly to cats, SAA, the inflammatory marker we regard as highly important, actually decreased. The mechanism, especially SIRT1, and the human data on cholesterol and CRP point in the same general direction.

Still, this remains a possibility, not a proven feline kidney-disease therapy. The feline data are promising, but limited. More direct studies in cats with kidney disease are needed.

It is also worth noting that the main feline study was conducted by Dr. Arai and Dr. Kobayashi, who serve as scientific advisors to Greycoat Research. On that basis, quercetin is one of the ingredients Greycoat Research is evaluating and incorporating into its product design. 

The findings discussed in this article reflect associations, mechanisms, and early translational evidence rather than confirmed efficacy in cats with kidney disease. Please consult a veterinarian before starting any supplementation protocol.

 < References >

1. Kobayashi M, Okada Y, Ueno H, Mizorogi T, Ohara K, Kawasumi K, Suruga K, Kadokura K, Ohnishi Y, Arai T. Effects of Supplementation with Anti-Inflammatory Compound Extracted from Herbs in Healthy and Obese Cats. Vet Med (Auckl). 2020;11:39-44.

2. Cui Z et al. Therapeutic application of quercetin in aging-related disease: SIRT1 as a potential mechanism. Front Immunol. 2022;13:943321.

3. Tabrizi R et al. The effects of quercetin supplementation on lipid profiles and inflammatory markers among patients with metabolic syndrome and related disorders. Crit Rev Food Sci Nutr. 2019;60(11):1855-1868.

4. Hickson LJ et al. Senolytics decrease senescent cells in humans: preliminary report from a clinical trial of dasatinib plus quercetin in individuals with diabetic kidney disease. eBioMedicine. 2019;47:446-456.

[Educational Disclaimer]

This article is for educational purposes only and is not a substitute for professional veterinary advice, diagnosis, or treatment. It is not intended to diagnose, treat, cure, or prevent any disease.

Please consult your veterinarian before making changes to your cat’s diet, supplements, or care routine.