QC: Understanding Why Endometriosis Lesions Grow, Bleed, And Change Color

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What if understanding how endometriosis builds its own blood supply could unlock safer, smarter treatment? We sit down with Professor Gaby Moawad—renowned robotic surgeon, educator, and leader in endometriosis care—to unpack the vascular engine that drives lesion growth, bleeding, and scarring. In five focused minutes, we translate complex molecular pathways into clear takeaways you can use to ask better questions and advocate for better care.

Dr. Moawad explains how hypoxia inside scarred tissue activates HIF alpha, which then boosts VEGF signaling to build new vessels. We explore how inflammation and locally produced estrogen amplify this process, why metalloproteinases (MMPs) cut space for vessels to form, and what immature pericytes have to do with leaky, bleeding lesions. He connects the dots from biology to the operating room: hypervascular lesions on MRI, the “powder burn” color changes created by hemosiderin, and the feedback loop that turns immune dysfunction into chronic pain and fibrosis.

We also touch on therapy frontiers. Anti-angiogenic drugs targeting VEGF show promise but raise concerns about wound healing and fertility. Dr. Moawad highlights where research is headed, including targeted delivery directly to lesions and cellular approaches that modulate endothelial progenitor cells. For anyone navigating diagnosis, imaging, fertility planning, or surgical decisions, this clear, science-backed overview offers a roadmap to discuss options with your care team and understand the trade-offs behind emerging treatments.

If this deep dive helped you see endometriosis through a sharper lens, follow the show, share it with someone who needs clarity, and leave a review so others can find it. Have a question you want answered fast? Send it our way and we’ll bring in the expert voice you need next.

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Episode Transcript

Alanna (00:00):
Life moves fast, and so should the answers to your
biggest questions.
Welcome to Endo Batteries QuickConnect, your direct line to
expert insights.
Short, powerful, and right tothe point.
You send in the questions, Ibring in the experts, and in
just five minutes, you get theknowledge you need.
No long episodes, no extra timeneeded.
And just remember, expertopinions shared here are for

(00:22):
general information and not forpersonalized medical advice.
Always consult your providerfor your case-specific guidance.
Got a question?
Send it in, and let's quicklyget you the answers.
I'm your host, Alanna, and it'stime to connect.
Today's guest is someone who istruly changing the landscape of

(00:45):
endometriosis care.
Professor Gaby Moawad is aglobally recognized leader in
robotic surgery andendometriosis management.
He's a board-certifiedgynecologic surgeon and the
founder of the Center forEndometriosis and Advanced
Pelvic Surgery in Washington,D.C.
Dr.
Moawad has dedicated his careerto advancing minimally invasive

(01:06):
and robotic techniques,combining surgical innovation
with deep, compassionate,patient-centered care.
As director of roboticgynecologic surgery and
associate professor at GeorgeWashington University, he's
trained surgeons worldwide andhelped redefine how we approach
complex pelvic disease.
He's been named Top Doctor inWashington, D.C.

(01:27):
for nearly a decade and hasauthored over 125 peer-reviewed
publications leading globalconversations on endometriosis
and surgical innovation.
It's an honor to sit down andwelcome a true pioneer and
advocate for better outcomes forwomen everywhere.
Please help me in welcoming Dr.

(01:48):
Gaby Moawad.
And lymphatic pathways and howthey might actually feed or
spread with endometriosis.

Dr. Moawad (02:02):
Well, if you you're looking for complexity, here's
your complex answer.
So there are there are a fewsubstances that I think every
endometriosis patient should atleast try to remember some names
or understand what they do inendometriosis.
Every endometriotic cell needsoxygen to grow, needs nutrients

(02:24):
to grow, and then needs bloodvessels to evacuate their waste.
This is part of almost everycell in the body rather than
endometriosis cells only.
So in endometriosis cells,there are what we call VEGF,
vascular endothelial growthfactor, and then VEGF receptors.

(02:46):
So there is a more a higherprevalence of VEGF that help
producing what we callangiogenesis and vasculogenesis.
Angiogenesis creating new bloodvessels.
So those lesions, because ofthe scarring that happens, they
are in a hypoxic state or pooroxygen comes there.

(03:09):
So they develop what we callhypoxia induced factor, HIF
alpha.
That what this produces, itupregulates the receptor to
attract more VEGF to producemore blood vessels.
So that HIF is a substance thatsays, I don't have any vessels

(03:30):
coming to bring me oxygen, solet's bring in more of the
vascular and telial growthfactor so they produce more
blood vessels.
Now, in addition to that, theinflammatory mediators,
interleukin A, tumor necrosisfactor, they also promote
inflammation and increase theVEGF in the endometriosis cells.

(03:54):
So you can see how the circlesis doing things, and the
estrogen is present in highconcentration in endometriosis
lesions because there is thearomatase.
They produce their ownestrogen, the endometriosis
cells.
Now add to this through allthat concoction, there is what

(04:14):
we call MMPs.
This is metalloproteinase.
These are substances that breakdown the matrix around the
cells for endometriosis, breakdown those proteins to create
space for blood vessels to form.
So now we see all those bloodvessels have space to form, they

(04:35):
start forming.
And we can see a higher densityeven on imaging of
endometriosis lesions when we dothe contrast on MRI, they're
hypervascularized.
Now, throughout that wholemedium, what happens?
Those inflammation startpromoting the bone marrow to
produce EPCs, EPC endothelialprogenitor cells.

(04:58):
So these are cells that comeand shear lead the formation of
vessels.
So you have a higher number ofthose cells, so everybody is
engaged to produce more vesselsin the endometriosis lesions.
Then we do say, oh,endometriosis lesions bleeds.

(05:19):
Why?
Because there is on every bloodvessel a lining of cells.
We can call them pericytes.
Peri means near, they lines,those sites mean cells, they
line the blood vessels.
So there is an immature supportof those pericytes.
That's why those blood vesselsare leaky, and that's why they

(05:40):
they tend to leak blood outside,and that's what they bleed.
So you can see how thatangiogenesis or the formation of
blood vessel is led byinflammation, by
hyperestrogenism, localhyperestrogenism in the lesions,
by all those substances createdto promote from the body, from

(06:01):
the bone marrow, to promotefurther formations of immature
cells that leads to bleeding andthen engage further the body to
inflame more.

Alanna (06:12):
Is that why we get variation in color for the
lesions as well?

Dr. Moawad (06:18):
Yes, yes, yes, yes.

Alanna (06:19):
And you know, we hear about the powder burn lesions,
but there's also a rainbow ofcolor in lesions.

Dr. Moawad (06:26):
So when the blood leaks from those vessels, it is
digested by the enzymes, andthey're part of the metabolites
of the digestion is hemofiderin,and they deposit there, and it
gives the color of purple orpowder burn lesion.
And then you can have adifferent level of vascular or
scarring because whenever youproduce inflammation, your body

(06:47):
reacts to scarring.
And since we have an immunedysfunction with endometriosis,
so the scarring is there is anover-reaction to the
inflammation with extensivescarring.

Alanna (06:59):
Yeah.

Dr. Moawad (07:00):
So it's mostly really well understood on the
molecular level, and this ishelp us a lot in trying to
figure out therapeuticapproaches.
So there have been trials thatdid target the VEGF or
anti-angiogenic therapeuticmedication.
These showed promising results,but they led to poor wound

(07:25):
healing, and then their impacton fertility is unknown.
So further study maybe aboutthe delivery method of those
substances, maybe directdelivery through the lesions,
might help improving withminimizing the systemic side
effects.
So when we understand what'scausing what, we can further our

(07:46):
research to try to help throughtargeted therapies or cellular
therapies for endometriosis.

Alanna (07:53):
That's a wrap for this quick connect.
I hope today's insights helpedyou move forward with more
clarity and confidence.
Do you have more questions?
Keep them coming.
Send them in, and I'll bringyou the expert answers.
You can send them in by usingthe link in the top of the
description of this podcastepisode or by emailing contact
at Indobattery.com or visitingthe Indobattery.com contact

(08:18):
page.
Until next time, keep feelingempowered through knowledge.